Alright Ladies and Gentlemen,
In my opinion, appetite suppression is one area where supplements work wonders. In addition, I also believe that appetite suppressants are generally underused. As we know, once an excess calorie is ingested, there is not a whole lot that can done to prevent fat gain. Despite all the advances in fat burners, simply avoiding the binges is of course a far superior solution. Below, I am listing the appetite suppressants that have worked great for me. The most helpful ones are those that show an immediate effect, because these can be taken when the need arises and eliminate most of the binge eating that could otherwise occur later during the day. However, other appetite suppressants that need to be taken regularly and will only show an effect after some time should also be included here IMO (I do not know of any in that category). Here is what worked for me:
Bitter Orange (tied for the #1 spot)
PseudoEphedrine, as contained in the 24 hour Sudafed (tied with B.Orange for the #1 spot)
Guarana
Regular Ephedrine HCL stacked with caffeine
Hoodia (this is hit or miss with me, some extracts work some do not)
Also, I really like Zappetite and Venom Hyperdrive but do not know which exact ingredients in these give them their potent appetite suppression benefits. Maybe it is the synergy of ingredients but I am just trying to identify the individual ingredients for this thread...
Please share your views.
Full Version: The Ultimate Appetite Suppression Thread
PEA (tolerance to stim effects does not seem to reduce appetite suppression)
Nicotine
Phenibut (Next-day suppression; not too useful with tolerance issues)
Tyrosine + ALCAR
5-HTP
Sibutramine (Studies below seem somewhat at odds. Doesn't a higher than expected REE imply thermogenesis?)
The effect of sibutramine on resting energy expenditure and adrenaline-induced thermogenesis in obese females.
Author: Walsh, K M : Leen, E : Lean, M E
Citation: Int-J-Obes-Relat-Metab-Disord. 1999 Oct; 23(10): 1009-15
Abstract: BACKGROUND: Sibutramine, an inhibitor of serotonin and noradrenaline uptake, reduces appetite to cause weight loss. This study tested the hypothesis that an increase in energy expenditure also contributes to this weight loss. In addition, the effects of sibutramine on adrenaline induced changes in heart rate and cardiac output were determined METHODS: Nineteen obese females randomly received either sibutramine 15 mg daily or placebo for 12 weeks along with dietary advice. Resting energy expenditure (REE) was measured and then energy expenditure was measured during a 30 min infusion of adrenaline (25 ng/min/kg IBW). Cardiac output and heart rate, measured by Duplex Colour Doppler ultrasonography, were similarly measured in the basal state and post adrenaline. All measurements were recorded at baseline and then after 12 weeks. RESULTS: Ten patients who received sibutramine reduced their weight by 8.1+/-3.8% while 9 placebo treated subjects reduced their weight by 5.1+/-4.4%, P=0.13. In absolute terms, REE decreased in placebo subjects from 1500+/-201 kcal/24 h to 1357+/-231 kcal/24 h (9.4+/-9.9%) and in sibutramine subjects from 1540+/-184 kcal/24 h to 1444+/-128 kcal/24 h (5.3+/-12.0%), P=0.77. The increased weight loss in the sibutramine group was associated with an increase in the FFM adjusted REE (2.2+/-16.1%) unlike the expected decrease (5.8+/-9.5%) in the placebo group (P=0.11). There was some suggestion (P=0.09) that the usual positive correlation between loss of weight and decline in REE was lost in the sibutramine group (r=-0.30) compared with placebo (r=0.35). There was a negative correlation between loss of FFM and decline in REE/kg FFM and (P=0.029) which was not evident in placebo (P=0.83). Adrenaline induced energy expenditure was similar in the two groups at the end of the 12 week period and there were no significant cardiovascular changes between the two groups. CONCLUSIONS: Sibutramine limits the decline in REE associated with weight loss, equivalent to about 100 kcal/d. This could allow greater numbers of people to maintain a greater degree of weight loss.
Ann Nutr Metab. 2008 Jan 30;52(1):17-23 [Epub ahead of print]
Related Articles, Links
The Effect of Sibutramine Intake on Resting and Exercise Physiological Responses.
Rotstein A, Inbar O, Vaisman N.
Department of Life Sciences, Zinman College, Wingate Institute, Netanya, Israel.
Aim: To evaluate the effect of a short-term sibutramine intake on energy expenditure and on physiological responses during rest, submaximal exercise and maximal exercise in obese women. Methods: Fifteen healthy obese female volunteers were randomly assigned to either a placebo (n = 6 - control) or sibutramine group (n = 9 - experimental) under double-blind conditions. Each subject was tested under resting conditions and then performed submaximal and maximal exercise tests. Subjects were retested under identical conditions following a 5-day administration of either sibutramine 10 mg.day(-1) or a placebo. All measurements (i.e. weight, body composition, resting energy expenditure, heart rate, respiratory exchange ratio, ventilation, oxygen consumption, carbon dioxide production, systolic blood pressure, diastolic blood pressure and blood lactate concentration) were analyzed using a 2-way ANOVA with repeated measures. Results: Only heart rate during submaximal exercise was significantly different (higher) following short-term sibutramine administration when compared to placebo (p < 0.05). Conclusions: These data suggest that a recommended daily dose of 10 mg sibutramine does not affect energy expenditure or other selected cardiopulmonary responses during rest, submaximal exercise or maximal exercise. It is, therefore, suggested that weight loss during sibutramine treatment in humans is achieved mostly via a decrease in energy intake rather than through an increase in energy expenditure and thermogenesis.
Nicotine
Phenibut (Next-day suppression; not too useful with tolerance issues)
Tyrosine + ALCAR
5-HTP
Sibutramine (Studies below seem somewhat at odds. Doesn't a higher than expected REE imply thermogenesis?)
The effect of sibutramine on resting energy expenditure and adrenaline-induced thermogenesis in obese females.
Author: Walsh, K M : Leen, E : Lean, M E
Citation: Int-J-Obes-Relat-Metab-Disord. 1999 Oct; 23(10): 1009-15
Abstract: BACKGROUND: Sibutramine, an inhibitor of serotonin and noradrenaline uptake, reduces appetite to cause weight loss. This study tested the hypothesis that an increase in energy expenditure also contributes to this weight loss. In addition, the effects of sibutramine on adrenaline induced changes in heart rate and cardiac output were determined METHODS: Nineteen obese females randomly received either sibutramine 15 mg daily or placebo for 12 weeks along with dietary advice. Resting energy expenditure (REE) was measured and then energy expenditure was measured during a 30 min infusion of adrenaline (25 ng/min/kg IBW). Cardiac output and heart rate, measured by Duplex Colour Doppler ultrasonography, were similarly measured in the basal state and post adrenaline. All measurements were recorded at baseline and then after 12 weeks. RESULTS: Ten patients who received sibutramine reduced their weight by 8.1+/-3.8% while 9 placebo treated subjects reduced their weight by 5.1+/-4.4%, P=0.13. In absolute terms, REE decreased in placebo subjects from 1500+/-201 kcal/24 h to 1357+/-231 kcal/24 h (9.4+/-9.9%) and in sibutramine subjects from 1540+/-184 kcal/24 h to 1444+/-128 kcal/24 h (5.3+/-12.0%), P=0.77. The increased weight loss in the sibutramine group was associated with an increase in the FFM adjusted REE (2.2+/-16.1%) unlike the expected decrease (5.8+/-9.5%) in the placebo group (P=0.11). There was some suggestion (P=0.09) that the usual positive correlation between loss of weight and decline in REE was lost in the sibutramine group (r=-0.30) compared with placebo (r=0.35). There was a negative correlation between loss of FFM and decline in REE/kg FFM and (P=0.029) which was not evident in placebo (P=0.83). Adrenaline induced energy expenditure was similar in the two groups at the end of the 12 week period and there were no significant cardiovascular changes between the two groups. CONCLUSIONS: Sibutramine limits the decline in REE associated with weight loss, equivalent to about 100 kcal/d. This could allow greater numbers of people to maintain a greater degree of weight loss.
Ann Nutr Metab. 2008 Jan 30;52(1):17-23 [Epub ahead of print]
Related Articles, Links
The Effect of Sibutramine Intake on Resting and Exercise Physiological Responses.
Rotstein A, Inbar O, Vaisman N.
Department of Life Sciences, Zinman College, Wingate Institute, Netanya, Israel.
Aim: To evaluate the effect of a short-term sibutramine intake on energy expenditure and on physiological responses during rest, submaximal exercise and maximal exercise in obese women. Methods: Fifteen healthy obese female volunteers were randomly assigned to either a placebo (n = 6 - control) or sibutramine group (n = 9 - experimental) under double-blind conditions. Each subject was tested under resting conditions and then performed submaximal and maximal exercise tests. Subjects were retested under identical conditions following a 5-day administration of either sibutramine 10 mg.day(-1) or a placebo. All measurements (i.e. weight, body composition, resting energy expenditure, heart rate, respiratory exchange ratio, ventilation, oxygen consumption, carbon dioxide production, systolic blood pressure, diastolic blood pressure and blood lactate concentration) were analyzed using a 2-way ANOVA with repeated measures. Results: Only heart rate during submaximal exercise was significantly different (higher) following short-term sibutramine administration when compared to placebo (p < 0.05). Conclusions: These data suggest that a recommended daily dose of 10 mg sibutramine does not affect energy expenditure or other selected cardiopulmonary responses during rest, submaximal exercise or maximal exercise. It is, therefore, suggested that weight loss during sibutramine treatment in humans is achieved mostly via a decrease in energy intake rather than through an increase in energy expenditure and thermogenesis.
Korean Pine Nut (Pinus koraiensis) / pinolenic acid
Loders Croklaan sells PinnoThin, Jenny Causey works for Loders
Korean pine nut fatty acids induce satiety producing
hormone release in overweight human
volunteers
Causey JL. Korean pine nut fatty acids induce satiety-producing hormone release in overweight human volunteers. Paper presented at: American Chemical Society National Meeting & Exposition; March 26-30, 2006; Atlanta, GA. AGFD 117
Jennifer L. Causey, Lipid Nutrition, a Division of Loders
Croklaan, 24708 West Durkee Road, Channahon, IL
60410, jennifer.causey@croklaan.com
Obesity and overweight are conditions that affect over half of the US population. Numerous treatment options are available to help combat weight gain, including reduction of food intake by appetite suppression. Numerous food-associated hormones are secreted by enteroendocrine cells of the gastrointestinal tract in response to the macronutrient composition of a meal. These hormones act as circulating ligands in the peripheral and central nervous system and result in behavioral modifications such as food intake reduction. Collectively, gastrointestinal
signals that direct the nervous system to reduce food intake are known as “satiety signals”. The most well-known of these hormones are cholecystokinin (CCK), and glucagon-like peptide (GLP-1). The Korean Pine Nut (Pinus koraiensis) contains significant levels of certain fatty acids shown in vitro to induce the release of CCK in STC-1 enteroendocrine cells. This pine nut oil (PinnoThin) was commercially produced and subsequently investigated in 18 overweight women (BMI=25- 30 kg/m3) who participated in a randomized, doubleblind placebo-controlled trial designed to measure aspects of satiety. Volunteers received 3 grams active or olive oil placebo in the form of gel capsules immediately before a carbohydrate test meal. Hormone measures (CCK, GLP-1, PYY peptide, and ghrelin) were taken at 0, 30, 60, 90, 120, 180, and 240 minutes following supplementation. Subjective appetite-related measures were also recorded at each time interval. The study demonstrated a significant increase in the satiety hormones CCK and GLP-1 over 4-hours (p<0.0001): PYY and ghrelin levels were not significantly different from placebo. Subjective appetite scores followed a similarly significant pattern. “Desire to eat” and “prospective food intake” as measured on a visual analog scale (VAS) were 29 and 36% lower that placebo, respectively. These results are
discussed in the context of potential weight management options with naturally-derived, lipid-based ingredients such as PinnoThin.
_______________________________________
On a related note:
The role of the AMP-activated protein kinase in the regulation of energy homeostasis
Novartis Found Symp. 2007;286:72-81; discussion 81-5, 162-3, 196-203.
The role of the AMP-activated protein kinase in the regulation of energy homeostasis.
Carling D.
Cellular Stress Group, MRC Clinical Sciences Centre, Imperial College, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK.
AMP-activated protein kinase (AMPK) is the downstream component of a protein kinase cascade that plays a major role in maintaining energy homeostasis. Within individual cells, AMPK is activated by a rise in the AMP:ATP ratio that occurs following a fall in ATP levels. AMPK is also regulated by the adipokines, adiponectin and leptin, hormones that are secreted from adipocytes. Activation of AMPK requires phosphorylation of threonine 172 within the catalytic subunit by either LKB1 or calcium/calmodulin dependent protein kinase kinase beta (CaMKKbeta). AMPK regulates a wide range of metabolic pathways, including fatty acid oxidation, fatty acid synthesis, glycolysis and gluconeogenesis. In peripheral tissues, activation of AMPK leads to responses that are beneficial in counteracting the deleterious effects that arise in the metabolic syndrome. Recent studies have demonstrated that modulation of AMPK activity in the hypothalamus plays a role in feeding. A decrease in hypothalamic AMPK activity is associated with decreased feeding, whereas activation of AMPK leads to increased food intake. Furthermore, signalling pathways in the hypothalamus lead to changes in AMPK activity in peripheral tissues, such as skeletal muscle, via the sympathetic nervous system (SNS). AMPK, therefore, provides a mechanism for monitoring changes in energy metabolism within individual cells and at the level of the whole body.
Loders Croklaan sells PinnoThin, Jenny Causey works for Loders
Korean pine nut fatty acids induce satiety producing
hormone release in overweight human
volunteers
Causey JL. Korean pine nut fatty acids induce satiety-producing hormone release in overweight human volunteers. Paper presented at: American Chemical Society National Meeting & Exposition; March 26-30, 2006; Atlanta, GA. AGFD 117
Jennifer L. Causey, Lipid Nutrition, a Division of Loders
Croklaan, 24708 West Durkee Road, Channahon, IL
60410, jennifer.causey@croklaan.com
Obesity and overweight are conditions that affect over half of the US population. Numerous treatment options are available to help combat weight gain, including reduction of food intake by appetite suppression. Numerous food-associated hormones are secreted by enteroendocrine cells of the gastrointestinal tract in response to the macronutrient composition of a meal. These hormones act as circulating ligands in the peripheral and central nervous system and result in behavioral modifications such as food intake reduction. Collectively, gastrointestinal
signals that direct the nervous system to reduce food intake are known as “satiety signals”. The most well-known of these hormones are cholecystokinin (CCK), and glucagon-like peptide (GLP-1). The Korean Pine Nut (Pinus koraiensis) contains significant levels of certain fatty acids shown in vitro to induce the release of CCK in STC-1 enteroendocrine cells. This pine nut oil (PinnoThin) was commercially produced and subsequently investigated in 18 overweight women (BMI=25- 30 kg/m3) who participated in a randomized, doubleblind placebo-controlled trial designed to measure aspects of satiety. Volunteers received 3 grams active or olive oil placebo in the form of gel capsules immediately before a carbohydrate test meal. Hormone measures (CCK, GLP-1, PYY peptide, and ghrelin) were taken at 0, 30, 60, 90, 120, 180, and 240 minutes following supplementation. Subjective appetite-related measures were also recorded at each time interval. The study demonstrated a significant increase in the satiety hormones CCK and GLP-1 over 4-hours (p<0.0001): PYY and ghrelin levels were not significantly different from placebo. Subjective appetite scores followed a similarly significant pattern. “Desire to eat” and “prospective food intake” as measured on a visual analog scale (VAS) were 29 and 36% lower that placebo, respectively. These results are
discussed in the context of potential weight management options with naturally-derived, lipid-based ingredients such as PinnoThin.
_______________________________________
On a related note:
The role of the AMP-activated protein kinase in the regulation of energy homeostasis
Novartis Found Symp. 2007;286:72-81; discussion 81-5, 162-3, 196-203.
The role of the AMP-activated protein kinase in the regulation of energy homeostasis.
Carling D.
Cellular Stress Group, MRC Clinical Sciences Centre, Imperial College, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK.
AMP-activated protein kinase (AMPK) is the downstream component of a protein kinase cascade that plays a major role in maintaining energy homeostasis. Within individual cells, AMPK is activated by a rise in the AMP:ATP ratio that occurs following a fall in ATP levels. AMPK is also regulated by the adipokines, adiponectin and leptin, hormones that are secreted from adipocytes. Activation of AMPK requires phosphorylation of threonine 172 within the catalytic subunit by either LKB1 or calcium/calmodulin dependent protein kinase kinase beta (CaMKKbeta). AMPK regulates a wide range of metabolic pathways, including fatty acid oxidation, fatty acid synthesis, glycolysis and gluconeogenesis. In peripheral tissues, activation of AMPK leads to responses that are beneficial in counteracting the deleterious effects that arise in the metabolic syndrome. Recent studies have demonstrated that modulation of AMPK activity in the hypothalamus plays a role in feeding. A decrease in hypothalamic AMPK activity is associated with decreased feeding, whereas activation of AMPK leads to increased food intake. Furthermore, signalling pathways in the hypothalamus lead to changes in AMPK activity in peripheral tissues, such as skeletal muscle, via the sympathetic nervous system (SNS). AMPK, therefore, provides a mechanism for monitoring changes in energy metabolism within individual cells and at the level of the whole body.
NOw brand Hoodia works for me, though Frangible raised some disturbing questions about possible liver toxicity in an e-mail (see below)
I've got a bottle of the pine nut stuff, and not sure it did anything so far. Hoodia ain't subtle if it works for you.
http://query.nytimes.com/gst/fullpage.html...757C0A9639C8B63
A Popular Pill's Hidden Danger
Published: April 26, 2005
To the Editor:
Re ''An Appetite Killer for a Killer Appetite? Not Yet'' (April 19): Having spent several years leading the struggle to develop hoodia at Pfizer, I can justly reinforce the cautionary note in the article.
An early clinical trial indeed showed that hoodia could be a potent appetite suppressant. But there were indications of unwanted effects on the liver caused by other components, which could not be easily removed from the supplement.
Clearly, hoodia has a long way to go before it can earn approval from the Food and Drug Administration. Until safer formulations are developed, dieters should be wary of using it.
JASJIT S. BINDRA
Groton, Conn.
I've got a bottle of the pine nut stuff, and not sure it did anything so far. Hoodia ain't subtle if it works for you.
http://query.nytimes.com/gst/fullpage.html...757C0A9639C8B63
A Popular Pill's Hidden Danger
Published: April 26, 2005
To the Editor:
Re ''An Appetite Killer for a Killer Appetite? Not Yet'' (April 19): Having spent several years leading the struggle to develop hoodia at Pfizer, I can justly reinforce the cautionary note in the article.
An early clinical trial indeed showed that hoodia could be a potent appetite suppressant. But there were indications of unwanted effects on the liver caused by other components, which could not be easily removed from the supplement.
Clearly, hoodia has a long way to go before it can earn approval from the Food and Drug Administration. Until safer formulations are developed, dieters should be wary of using it.
JASJIT S. BINDRA
Groton, Conn.
There are also some issues with certain Hoodia products containing little/none of the active ingredient P57AS3.
P57AS3 is a steroidal glycoside btw, if that help to explain the liver issues.
P57AS3 is a steroidal glycoside btw, if that help to explain the liver issues.
I've recently tried LEF's pine nut oil while on Rimonbant at 20mg without much to say,both were done with as of last week.
I am now using Zappetite,which puts me on cloud 9 (sceletium content) along with another pine nut oil,PinoSlim.
I'm on a modified intermittent fast (eating window of 6 hours at night with casien shakes throughout the day) and cravings are much more controllable and I only eat when needed.I think a lot of this has to do with the mood elevation from sceletium,I heart this shit.
I am now using Zappetite,which puts me on cloud 9 (sceletium content) along with another pine nut oil,PinoSlim.
I'm on a modified intermittent fast (eating window of 6 hours at night with casien shakes throughout the day) and cravings are much more controllable and I only eat when needed.I think a lot of this has to do with the mood elevation from sceletium,I heart this shit.
Lots of great research on capsaicin.
Int J Obes (Lond). 2005 Jun;29(6):682-8. Links
Sensory and gastrointestinal satiety effects of capsaicin on food intake.Westerterp-Plantenga MS, Smeets A, Lejeune MP.
Department of Human Biology, Maastricht University, Maastricht, The Netherlands. m.westerterp.hb.unimaas.nl
BACKGROUND: Decreased appetite and increased energy expenditure after oral consumption of red pepper has been shown. OBJECTIVE: The aim of the present study was to assess the relative oral and gastrointestinal contribution to capsaicin-induced satiety and its effects on food intake or macronutrient selection. METHODS: For 24 subjects (12 men and 12 women; age: 35+/-10 y; BMI: 25.0+/-2.4 kg/m2; range 20-30), 16 h food intake was assessed four times during 2 consecutive days by offering macronutrient-specific buffets and boxes with snacks, in our laboratory restaurant. At 30 min before each meal, 0.9 g red pepper (0.25% capsaicin; 80,000 Scoville Thermal Units) or a placebo was offered in either tomato juice or in two capsules that were swallowed with tomato juice. Hunger and satiety were recorded using Visual Analogue Scales. RESULTS: Average daily energy intake in the placebo condition was 11.5+/-1.0 MJ/d for the men and 9.4+/-0.8 MJ/d for the women. After capsaicin capsules, energy intake was 10.4+/-0.6 and 8.3+/-0.5 MJ/d (P<0.01); after capsaicin in tomato juice, it was 9.9+/-0.7 and 7.9+/-0.5 MJ/d, respectively (compared to placebo: P<0.001; compared to capsaicin in capsules: P<0.05). En % from carbohydrate/protein/fat (C/P/F): changed from 46+/-3/15+/-1/39+/-2 to 52+/-4/15+/-1/33+/-2 en% (P<0.01) in the men, and from 48+/-4/14+/-2/38+/-3 to 42+/-4/14+/-2/32+/-3 en% (P<0.01) in the women, in both capsaicin conditions. Satiety (area under the curve) increased from 689 to 757 mmh in the men and from 712 to 806 mmh in the women, both (P<0.01). Only in the oral exposure condition was the reduction in energy intake and the increase in satiety related to perceived spiciness. CONCLUSION: In the short term, both oral and gastrointestinal exposure to capsaicin increased satiety and reduced energy and fat intake; the stronger reduction with oral exposure suggests a sensory effect of capsaicin.
PMID: 15611784 [PubMed - indexed for MEDLINE]
Int J Obes (Lond). 2005 Jun;29(6):682-8. Links
Sensory and gastrointestinal satiety effects of capsaicin on food intake.Westerterp-Plantenga MS, Smeets A, Lejeune MP.
Department of Human Biology, Maastricht University, Maastricht, The Netherlands. m.westerterp.hb.unimaas.nl
BACKGROUND: Decreased appetite and increased energy expenditure after oral consumption of red pepper has been shown. OBJECTIVE: The aim of the present study was to assess the relative oral and gastrointestinal contribution to capsaicin-induced satiety and its effects on food intake or macronutrient selection. METHODS: For 24 subjects (12 men and 12 women; age: 35+/-10 y; BMI: 25.0+/-2.4 kg/m2; range 20-30), 16 h food intake was assessed four times during 2 consecutive days by offering macronutrient-specific buffets and boxes with snacks, in our laboratory restaurant. At 30 min before each meal, 0.9 g red pepper (0.25% capsaicin; 80,000 Scoville Thermal Units) or a placebo was offered in either tomato juice or in two capsules that were swallowed with tomato juice. Hunger and satiety were recorded using Visual Analogue Scales. RESULTS: Average daily energy intake in the placebo condition was 11.5+/-1.0 MJ/d for the men and 9.4+/-0.8 MJ/d for the women. After capsaicin capsules, energy intake was 10.4+/-0.6 and 8.3+/-0.5 MJ/d (P<0.01); after capsaicin in tomato juice, it was 9.9+/-0.7 and 7.9+/-0.5 MJ/d, respectively (compared to placebo: P<0.001; compared to capsaicin in capsules: P<0.05). En % from carbohydrate/protein/fat (C/P/F): changed from 46+/-3/15+/-1/39+/-2 to 52+/-4/15+/-1/33+/-2 en% (P<0.01) in the men, and from 48+/-4/14+/-2/38+/-3 to 42+/-4/14+/-2/32+/-3 en% (P<0.01) in the women, in both capsaicin conditions. Satiety (area under the curve) increased from 689 to 757 mmh in the men and from 712 to 806 mmh in the women, both (P<0.01). Only in the oral exposure condition was the reduction in energy intake and the increase in satiety related to perceived spiciness. CONCLUSION: In the short term, both oral and gastrointestinal exposure to capsaicin increased satiety and reduced energy and fat intake; the stronger reduction with oral exposure suggests a sensory effect of capsaicin.
PMID: 15611784 [PubMed - indexed for MEDLINE]
venom - hoodia + synephrine combine to almost make me want to puke at even the mere thought of eating for the first 2 hours.
DCP seems to kill my hunger too.... Much more subtly though
DCP seems to kill my hunger too.... Much more subtly though
I get the opposite from DCP. It seems to increase my appetite whenever I use it.
Xanthum gum and/or inulin in a protein shake seems to increase satiety for me a great deal.
Xanthum gum and/or inulin in a protein shake seems to increase satiety for me a great deal.
20oz of water and 12 Metamucil caps?
ha j/k (maybe)
I know what you guys are gonna say, but Xendrine EFX really helped blunt my hunger. Almost too much.
ha j/k (maybe)
I know what you guys are gonna say, but Xendrine EFX really helped blunt my hunger. Almost too much.
The problem for me with most appetite suppressants is that anymore if it's potent enough to kill my appetite it's potent enough to make me feel like crap.
ephedrine used to feel like meth to me, I'd fly on it. Now I just snap at everyone and actually end up eating more shortly after because of the hypoglycemia.
ephedrine used to feel like meth to me, I'd fly on it. Now I just snap at everyone and actually end up eating more shortly after because of the hypoglycemia.
Very expensive drug, although others in it's class (glycosyltransferases, ER alpha-glucosidases inhibitor) may hold some promise.
N-butyldeoxynojirimycin causes weight loss as a result of appetite suppression in lean and obese mice
Abstract
Aim: To determine the mechanism of weight loss caused by high doses of N-butyldeoxynojirimycin (NB-DNJ) in healthy lean and leptindeficient obese (ob/ob) mice.
Methods: Healthy lean and obese mice were treated with NB-DNJ by the following methods: admixed with their diet, delivered by subcutaneously implanted mini-pumps or by intraperitoneal or intracerebroventricular (ICV) injection. Daily changes in body weight and food intake were recorded during the experimental period. The effect of NB-DNJ treatment on subcutaneous adipose tissue and on epididymal fat pads was measured.
Results: Lean mice treated with NB-DNJ, admixed with their diet, lost weight in the form of adipose tissue. This resulted in a 40% reduction in skin thickness (control, 358 11 μm; NB-DNJ treated 203 6 μm) and a reduction in epididymal fat pad weights after 5 weeks of treatment at 2400 mg/kg/day (control, 0.0154 0.001; NB-DNJ treated, 0.0026 0.0005 as ratios of fat pad weight to total body weight). Following the depletion of adipose tissue mass, the mice grew normally and did not have any reduction in lean mass. Obese mice treated with NB-DNJ also lost weight or gained weight at a greatly reduced rate compared with non-treated controls. Body weights at 6 months of age were: lean control, 29.10 1.15 g; lean NB-DNJ treated, 22.73 0.29 g; obese control, 63.25 1.5 g; obese NB-DNJ treated from 5 weeks of age, 35.30 1.68 g; obese NB-DNJ treated from 12 weeks of age, 38.84 1.26 g. Both the lean and obese groups of mice treated with NB-DNJ ate up to 30% less than untreated controls. Daily food intake (powder diet) were: lean control, 4.15 0.54 g; obese control, 4.14 0.2 g; lean NB-DNJ treated 2.9 0.37 g; obese NB-DNJ treated, 2.88 0.47 g. Mice treated with the N-substituted galactose imino sugar analogue, N-butyldeoxygalactonojirimycin (NB-DGJ) did not lose weight. Mice experienced similar weight loss or lack of weight gain when fed a restricted diet that mimics the drug-induced level of food consumption. Delivery of 2 nmol NB-DNJ by ICV injection into lean mice also caused similar reductions in food intake. Food intake: saline vehicle, 4.30 0.12 g; NB-DNJ, 3.37 0.19 g; NB-DGJ, 4.03 0.16 g; 2-deoxyglucose, 4.7 0.15 g.
Conclusion: NB-DNJ causes weight loss as a result of reduced food consumption due to central appetite suppression.
N-butyldeoxynojirimycin causes weight loss as a result of appetite suppression in lean and obese mice
Abstract
Aim: To determine the mechanism of weight loss caused by high doses of N-butyldeoxynojirimycin (NB-DNJ) in healthy lean and leptindeficient obese (ob/ob) mice.
Methods: Healthy lean and obese mice were treated with NB-DNJ by the following methods: admixed with their diet, delivered by subcutaneously implanted mini-pumps or by intraperitoneal or intracerebroventricular (ICV) injection. Daily changes in body weight and food intake were recorded during the experimental period. The effect of NB-DNJ treatment on subcutaneous adipose tissue and on epididymal fat pads was measured.
Results: Lean mice treated with NB-DNJ, admixed with their diet, lost weight in the form of adipose tissue. This resulted in a 40% reduction in skin thickness (control, 358 11 μm; NB-DNJ treated 203 6 μm) and a reduction in epididymal fat pad weights after 5 weeks of treatment at 2400 mg/kg/day (control, 0.0154 0.001; NB-DNJ treated, 0.0026 0.0005 as ratios of fat pad weight to total body weight). Following the depletion of adipose tissue mass, the mice grew normally and did not have any reduction in lean mass. Obese mice treated with NB-DNJ also lost weight or gained weight at a greatly reduced rate compared with non-treated controls. Body weights at 6 months of age were: lean control, 29.10 1.15 g; lean NB-DNJ treated, 22.73 0.29 g; obese control, 63.25 1.5 g; obese NB-DNJ treated from 5 weeks of age, 35.30 1.68 g; obese NB-DNJ treated from 12 weeks of age, 38.84 1.26 g. Both the lean and obese groups of mice treated with NB-DNJ ate up to 30% less than untreated controls. Daily food intake (powder diet) were: lean control, 4.15 0.54 g; obese control, 4.14 0.2 g; lean NB-DNJ treated 2.9 0.37 g; obese NB-DNJ treated, 2.88 0.47 g. Mice treated with the N-substituted galactose imino sugar analogue, N-butyldeoxygalactonojirimycin (NB-DGJ) did not lose weight. Mice experienced similar weight loss or lack of weight gain when fed a restricted diet that mimics the drug-induced level of food consumption. Delivery of 2 nmol NB-DNJ by ICV injection into lean mice also caused similar reductions in food intake. Food intake: saline vehicle, 4.30 0.12 g; NB-DNJ, 3.37 0.19 g; NB-DGJ, 4.03 0.16 g; 2-deoxyglucose, 4.7 0.15 g.
Conclusion: NB-DNJ causes weight loss as a result of reduced food consumption due to central appetite suppression.
Spiking insulin with non-caloric sweetners, say with a prolonged infusion of acesulfame K, could reduce ghrelin levels and increase insulin (and by extension - leptin) levels. Of course, high insulin tends to correlate with hunger, at least anecdotally. So assumng absence of leptin resistance (i.e. non-obese, non-hyperinsulemic, low serum TAG's) this may have some merit (?). Just throwing stuff against the wall to see what sticks...
Ghrelin rises in anticipation of a feeding, making IF/low meal frequency a logical choice for appetite management.
Horm Metab Res. 1987 Jun;19(6):233-8.Related Articles, Links
The effect of artificial sweetener on insulin secretion. 1. The effect of acesulfame K on insulin secretion in the rat (studies in vivo).
Liang Y, Steinbach G, Maier V, Pfeiffer EF.
Acesulfame K is an artificial sweetener which has been used in the food industry for some years. As yet no metabolic effects have been reported. It was reported that the sweetener can induce a cephalic phase of insulin secretion. To analyse the mechanism of this phenomenon, we studied the effect of Acesulfame K on insulin secretion in vivo. Male Wistar rats, weighing 250-300 g were fasted overnight and anaesthetized with phenobarbital. A silicon catheter was inserted into the right cervical vein for injection of test substances and for obtaining blood samples. In some experiments, another catheter was inserted into the left cervical vein for continuous infusion. Blood samples were drawn at 0, 5, 10, 15, 30 and 60 min after injection, and at -10, 0, 10, 20, 30, 40, 60, 80, 100 and 120 min after the infusion started. Injection of Acesulfame K (150 mg/kg body weight) increased the plasma insulin concentration at 5 min from 27.3 +/- 3.0 microU/ml to 58.6 +/- 4.2 microU/ml without any significant change in the blood glucose. Infusion of Acesulfame K (20 mg/kg body weight/min) for one hour maintained the insulin concentration at a high level (about 85-100 microU/ml) during this period, and at the same time blood glucose was gradually reduced from 103.0 +/- 7.3 to 72.0 +/- 7.2 mg/dl. When using different amounts of Acesulfame K, the insulin secretion was stimulated in a dose-dependent fashion. The effect of Acesulfame K on insulin secretion was similar to that observed by injecting or infusing the same doses of glucose (150 mg/kg) body weight for injection and 20 mg/kg body weight/min for infusion), except that no hyperglycemia was observed with Acesulfame K.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Physiol Gastrointest Liver Physiol. 2008 Jan 10 [Epub ahead of print]
Related Articles
Possible entrainment of ghrelin to habitual meal patterns in humans.
Frecka JM, Mattes RD.
Foods and Nutrition, Purdue University, West Lafayette, Indiana, United States.
Ghrelin is reportedly a meal-initiation signal based on observations that concentrations increase before meals coincident with rising hunger. However, evidence that ghrelin peaks vary with feeding schedules suggests it rises in anticipation of an expected meal, rather than eliciting feeding. To explore the entrainment of ghrelin profiles, this study investigated the association between varying habitual meal patterns and plasma ghrelin concentrations. Lean and obese adults following either a short intermeal interval (SII) pattern, with 2.5-3.5 hours between their habitual breakfast and lunch times, or a long intermeal interval (LII) pattern, with 5.5-6.5 hours between these eating occasions, participated. Food intake and appetite were recorded for 2 baseline days. On the subsequent test day, blood samples were collected over 8 hours while participants ate a breakfast and lunch matched to their customary meals and pattern. Appetite ratings were obtained and ghrelin, insulin, glucose, and leptin concentrations were measured. Peak ghrelin concentrations differed significantly by group and occurred prior to each groups' respective lunch time. Ghrelin concentrations directly correlated with subjective hunger. This association was stronger when hunger preceded ghrelin; a pattern inconsistent with ghrelin causing the hunger rise. Ghrelin concentrations were inversely correlated with insulin, and peak insulin concentrations preceded nadir ghrelin concentrations postprandially. Ghrelin concentrations periprandially, and over the entire test session, did not differ by meal group, likely due to similar intakes between groups. These data demonstrate the timing of ghrelin peaks is related to habitual meal patterns and may rise in anticipation of eating rather than eliciting feeding.
Leptin and its metabolic interactions an update
Anubhuti and Sarika Arora
Department of Biochemistry, GB Pant Hospital, New Delhi, India
As mentioned earlier, insulin increases leptin production indirectly through its effects to increase glucose utilization
and oxidative glucose metabolism in adipocytes [169] at the transcriptional level [170] (figure 3).
Ghrelin rises in anticipation of a feeding, making IF/low meal frequency a logical choice for appetite management.
Horm Metab Res. 1987 Jun;19(6):233-8.Related Articles, Links
The effect of artificial sweetener on insulin secretion. 1. The effect of acesulfame K on insulin secretion in the rat (studies in vivo).
Liang Y, Steinbach G, Maier V, Pfeiffer EF.
Acesulfame K is an artificial sweetener which has been used in the food industry for some years. As yet no metabolic effects have been reported. It was reported that the sweetener can induce a cephalic phase of insulin secretion. To analyse the mechanism of this phenomenon, we studied the effect of Acesulfame K on insulin secretion in vivo. Male Wistar rats, weighing 250-300 g were fasted overnight and anaesthetized with phenobarbital. A silicon catheter was inserted into the right cervical vein for injection of test substances and for obtaining blood samples. In some experiments, another catheter was inserted into the left cervical vein for continuous infusion. Blood samples were drawn at 0, 5, 10, 15, 30 and 60 min after injection, and at -10, 0, 10, 20, 30, 40, 60, 80, 100 and 120 min after the infusion started. Injection of Acesulfame K (150 mg/kg body weight) increased the plasma insulin concentration at 5 min from 27.3 +/- 3.0 microU/ml to 58.6 +/- 4.2 microU/ml without any significant change in the blood glucose. Infusion of Acesulfame K (20 mg/kg body weight/min) for one hour maintained the insulin concentration at a high level (about 85-100 microU/ml) during this period, and at the same time blood glucose was gradually reduced from 103.0 +/- 7.3 to 72.0 +/- 7.2 mg/dl. When using different amounts of Acesulfame K, the insulin secretion was stimulated in a dose-dependent fashion. The effect of Acesulfame K on insulin secretion was similar to that observed by injecting or infusing the same doses of glucose (150 mg/kg) body weight for injection and 20 mg/kg body weight/min for infusion), except that no hyperglycemia was observed with Acesulfame K.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Physiol Gastrointest Liver Physiol. 2008 Jan 10 [Epub ahead of print]
Related Articles
Possible entrainment of ghrelin to habitual meal patterns in humans.
Frecka JM, Mattes RD.
Foods and Nutrition, Purdue University, West Lafayette, Indiana, United States.
Ghrelin is reportedly a meal-initiation signal based on observations that concentrations increase before meals coincident with rising hunger. However, evidence that ghrelin peaks vary with feeding schedules suggests it rises in anticipation of an expected meal, rather than eliciting feeding. To explore the entrainment of ghrelin profiles, this study investigated the association between varying habitual meal patterns and plasma ghrelin concentrations. Lean and obese adults following either a short intermeal interval (SII) pattern, with 2.5-3.5 hours between their habitual breakfast and lunch times, or a long intermeal interval (LII) pattern, with 5.5-6.5 hours between these eating occasions, participated. Food intake and appetite were recorded for 2 baseline days. On the subsequent test day, blood samples were collected over 8 hours while participants ate a breakfast and lunch matched to their customary meals and pattern. Appetite ratings were obtained and ghrelin, insulin, glucose, and leptin concentrations were measured. Peak ghrelin concentrations differed significantly by group and occurred prior to each groups' respective lunch time. Ghrelin concentrations directly correlated with subjective hunger. This association was stronger when hunger preceded ghrelin; a pattern inconsistent with ghrelin causing the hunger rise. Ghrelin concentrations were inversely correlated with insulin, and peak insulin concentrations preceded nadir ghrelin concentrations postprandially. Ghrelin concentrations periprandially, and over the entire test session, did not differ by meal group, likely due to similar intakes between groups. These data demonstrate the timing of ghrelin peaks is related to habitual meal patterns and may rise in anticipation of eating rather than eliciting feeding.
Leptin and its metabolic interactions an update
Anubhuti and Sarika Arora
Department of Biochemistry, GB Pant Hospital, New Delhi, India
As mentioned earlier, insulin increases leptin production indirectly through its effects to increase glucose utilization
and oxidative glucose metabolism in adipocytes [169] at the transcriptional level [170] (figure 3).
2 caps amp and a energy drink, 16oz sobe adrenaline rush (sugar free) always did the trick.
QUOTE(Kimbo @ Feb 22 2008, 02:28 PM) [snapback]460317[/snapback]
I get the opposite from DCP. It seems to increase my appetite whenever I use it.
Really? Even with those delightful little raspberry burps?
Xanthum gum and/or inulin in a protein shake seems to increase satiety for me a great deal.
Really? Even with those delightful little raspberry burps?
Xanthum gum and/or inulin in a protein shake seems to increase satiety for me a great deal.
Inulin makes me crazy gassy. If I eat more than 1 "liveactive" cottage cheese or atkins bar I'm a walking fire hazard the next day. When I ate Dreamfields it just got downright dangerous.
Yohimbine + Ephedrine seems to work really well for suppression, as does nicotine.
So many things that work seem to have health side effects. PseudoEphedrine for one, caffeine for another. Others we don't know much about. The one thing that works for me with no side effects is to avoid simple carbs. Avoiding refined sugar and flour does the job. Food cravings go away or become less.
The red pepper angle sounds interesting. I wonder if you just capped some up would that work? I can't see putting that much on my food every day.
What's the active ingredient in bitter orange?
The red pepper angle sounds interesting. I wonder if you just capped some up would that work? I can't see putting that much on my food every day.
What's the active ingredient in bitter orange?
I sure would love something that didnt jack me up and wasnt a stim... Hoodia looks promising, but it seems really hit or miss. I know this summer I really can't go back to smoking, and would like to really cut out dipping, outside of those two I don't know what else really works. Going on EQ is going to kill me, so lets keep this thread rolling. Anymore feedback on Zappetite?
I don't like the stimulant route either.
The pine nut oils did'nt do anything for me, but Metformin works pretty well.
The pine nut oils did'nt do anything for me, but Metformin works pretty well.
QUOTE(speda1 @ Feb 23 2008, 02:54 PM) [snapback]460582[/snapback]
I don't like the stimulant route either.
The pine nut oils did'nt do anything for me, but Metformin works pretty well.
The pine nut oils did'nt do anything for me, but Metformin works pretty well.
Metformin are u serious? metaformin may increase insulin sensitivity by increasing peripheral utilization of glucose, but at the end i would think u would actualy gain weight.......if u real understand what i mean
QUOTE(x_muscle @ Feb 24 2008, 03:09 AM) [snapback]460626[/snapback]
Metformin are u serious? metaformin may increase insulin sensitivity by increasing peripheral utilization of glucose, but at the end i would think u would actualy gain weight.......if u real understand what i mean
IME, I agree.
QUOTE(D-termine @ Feb 23 2008, 05:33 PM) [snapback]460580[/snapback]
I sure would love something that didnt jack me up and wasnt a stim...
D have you tried 12h pseudoephedrine? Its got very little stimulant effect and is one of the more effective appetite suppressants I've tried.
I remember nicotine working wonders but I was taking other stuff at the time. I recently got some gum and its rather mild in effect.
I've tried one hoodia product and it seemed to work pretty good
The main problem I have is that I don't think to take another dose till I'm feeling hungry and then it can be too late.
the extended release pseudo sounds interesting.
I've tried one hoodia product and it seemed to work pretty good
The main problem I have is that I don't think to take another dose till I'm feeling hungry and then it can be too late.
the extended release pseudo sounds interesting.
QUOTE(x_muscle @ Feb 24 2008, 01:09 AM) [snapback]460626[/snapback]
Metformin are u serious? metaformin may increase insulin sensitivity by increasing peripheral utilization of glucose, but at the end i would think u would actualy gain weight.......if u real understand what i mean
I understand what the theory, but that is not happening in the real world. People lose weight on metformin.
QUOTE(speda1 @ Feb 24 2008, 11:00 AM) [snapback]460657[/snapback]
I understand what the theory, but that is not happening in the real world. People lose weight on metformin.
This makes perfect sense because, like exercise, it makes insulin more efficient so you end up with less of it in circulation making it easier for your body to access stored fat.
QUOTE(Supnut @ Feb 24 2008, 09:34 AM) [snapback]460649[/snapback]
the extended release pseudo sounds interesting.
NB, I'd steer clear of the 24 hour stuff...it may be just me, but I find that it exerts some localized effects in the colon that binds me up tight. Not an issue with the 12 hour version.
Nicotine, hands down. If the gum didn't work for you make sure to get the stronger 4mg pieces and park it like a dip. If that doesn't work, use two.
Try eating after that......
Try eating after that......
QUOTE(eclypz @ Feb 22 2008, 01:59 PM) [snapback]460345[/snapback]
ephedrine used to feel like meth to me, I'd fly on it. Now I just snap at everyone and actually end up eating more shortly after because of the hypoglycemia.
Don't B-agonists cause insulin resistance -> hyperglycemia?
QUOTE(Heavy_Lifter85 @ Feb 23 2008, 04:55 AM) [snapback]460494[/snapback]
As mentioned earlier, insulin increases leptin production indirectly through its effects to increase glucose utilization
and oxidative glucose metabolism in adipocytes [169] at the transcriptional level [170] (figure 3).
and oxidative glucose metabolism in adipocytes [169] at the transcriptional level [170] (figure 3).
I thought I had recently seen evidence that insulin increased leptin independent of glucose...
Potato protein can blunt appetite and improve satiety.
Am I the only one that never received any appetite suppression from nicotine? Neither dip nor gum ever helped. Similarly yohimbine caused nausea (like nicotine) which seemed to increase my drive to eat. Does the alpha-yohimbine have the same peripheral effects?
I wish someone would get a bulk Potato Protein extract....Satietin is the name if I remember.
Hoodia also was hit or miss, even within the same bottle. Worked great some times, not much other times.
Synephrine never did anything for me.
I wish someone would get a bulk Potato Protein extract....Satietin is the name if I remember.
Hoodia also was hit or miss, even within the same bottle. Worked great some times, not much other times.
Synephrine never did anything for me.
QUOTE(micro2000 @ Feb 24 2008, 01:23 PM) [snapback]460685[/snapback]
Am I the only one that never received any appetite suppression from nicotine? Neither dip nor gum ever helped. Similarly yohimbine caused nausea (like nicotine) which seemed to increase my drive to eat. Does the alpha-yohimbine have the same peripheral effects?
I wish someone would get a bulk Potato Protein extract....Satietin is the name if I remember.
Hoodia also was hit or miss, even within the same bottle. Worked great some times, not much other times.
Synephrine never did anything for me.
I wish someone would get a bulk Potato Protein extract....Satietin is the name if I remember.
Hoodia also was hit or miss, even within the same bottle. Worked great some times, not much other times.
Synephrine never did anything for me.
Nicotine gum makes me hungry.
QUOTE(speda1 @ Feb 24 2008, 08:00 AM) [snapback]460657[/snapback]
I understand what the theory, but that is not happening in the real world. People lose weight on metformin.
Doesn't metformin activate AMPK? I remember reading that its effects mimic caloric restriction.
Since Custom Nutrition now has guanidinopropionate, I am thinking that a decent fat loss stack might be some appetite suppressant combined with GPA, Sesamin and Fish oil.
QUOTE(micro2000 @ Feb 24 2008, 12:23 PM) [snapback]460709[/snapback]
Doesn't metformin activate AMPK? I remember reading that its effects mimic caloric restriction.
I wasn't aware that Metformin activated AMPK,any reference for this?
Can you be specific as to what the second sentence means?
FWIW,I've been using sceletium (kanna) and have been able to adjust to intermittent fasting with kcals at 10-12 b/w.
QUOTE(Colin @ Feb 24 2008, 12:33 PM) [snapback]460710[/snapback]
I wasn't aware that Metformin activated AMPK,any reference for this?
Can you be specific as to what the second sentence means?
FWIW,I've been using sceletium (kanna) and have been able to adjust to intermittent fasting with kcals at 10-12 b/w.
Can you be specific as to what the second sentence means?
FWIW,I've been using sceletium (kanna) and have been able to adjust to intermittent fasting with kcals at 10-12 b/w.
Diabetes. 2008 Feb;57(2):306-14. Epub 2007 Oct 1.
QUOTE
Metformin inhibits hepatic gluconeogenesis through AMP-activated protein kinase-dependent regulation of the orphan nuclear receptor SHP.Kim YD, Park KG, Lee YS, Park YY, Kim DK, Nedumaran B, Jang WG, Cho WJ, Ha J, Lee IK, Lee CH, Choi HS.
Hormone Research Center, School of Biological Sciences & Technology, Chonnam National University, Gwangju, 500-757, Republic of Korea.
OBJECTIVE: Metformin is an antidiabetic drug commonly used to treat type 2 diabetes. The aim of the study was to determine whether metformin regulates hepatic gluconeogenesis through the orphan nuclear receptor small heterodimer partner (SHP; NR0B2). RESEARCH DESIGN AND METHODS: We assessed the regulation of hepatic SHP gene expression by Northern blot analysis with metformin and adenovirus containing a constitutive active form of AMP-activated protein kinase (AMPK) (Ad-AMPK) and evaluated SHP, PEPCK, and G6Pase promoter activities via transient transfection assays in hepatocytes. Knockdown of SHP using siRNA SHP was conducted to characterize the metformin-induced inhibition of hepatic gluconeogenic gene expression in hepatocytes, and metformin-and adenovirus SHP (Ad-SHP)-mediated hepatic glucose production was measured in B6-Lep(ob/ob) mice. RESULTS: Hepatic SHP gene expression was induced by metformin, 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR), and Ad-AMPK. Metformin-induced SHP gene expression was abolished by adenovirus containing the dominant negative form of AMPK (Ad-DN-AMPK), as well as by compound C. Metformin inhibited hepatocyte nuclear factor-4alpha-or FoxA2-mediated promoter activity of PEPCK and G6Pase, and the inhibition was blocked with siRNA SHP. Additionally, SHP knockdown by adenovirus containing siRNA SHP inhibited metformin-mediated repression of cAMP/dexamethasone-induced hepatic gluconeogenic gene expression. Furthermore, oral administration of metformin increased SHP mRNA levels in B6-Lep(ob/ob) mice. Overexpression of SHP by Ad-SHP decreased blood glucose levels and hepatic gluconeogenic gene expression in B6-Lep(ob/ob) mice. CONCLUSIONS: We have concluded that metformin inhibits hepatic gluconeogenesis through AMPK-dependent regulation of SHP.
Hormone Research Center, School of Biological Sciences & Technology, Chonnam National University, Gwangju, 500-757, Republic of Korea.
OBJECTIVE: Metformin is an antidiabetic drug commonly used to treat type 2 diabetes. The aim of the study was to determine whether metformin regulates hepatic gluconeogenesis through the orphan nuclear receptor small heterodimer partner (SHP; NR0B2). RESEARCH DESIGN AND METHODS: We assessed the regulation of hepatic SHP gene expression by Northern blot analysis with metformin and adenovirus containing a constitutive active form of AMP-activated protein kinase (AMPK) (Ad-AMPK) and evaluated SHP, PEPCK, and G6Pase promoter activities via transient transfection assays in hepatocytes. Knockdown of SHP using siRNA SHP was conducted to characterize the metformin-induced inhibition of hepatic gluconeogenic gene expression in hepatocytes, and metformin-and adenovirus SHP (Ad-SHP)-mediated hepatic glucose production was measured in B6-Lep(ob/ob) mice. RESULTS: Hepatic SHP gene expression was induced by metformin, 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR), and Ad-AMPK. Metformin-induced SHP gene expression was abolished by adenovirus containing the dominant negative form of AMPK (Ad-DN-AMPK), as well as by compound C. Metformin inhibited hepatocyte nuclear factor-4alpha-or FoxA2-mediated promoter activity of PEPCK and G6Pase, and the inhibition was blocked with siRNA SHP. Additionally, SHP knockdown by adenovirus containing siRNA SHP inhibited metformin-mediated repression of cAMP/dexamethasone-induced hepatic gluconeogenic gene expression. Furthermore, oral administration of metformin increased SHP mRNA levels in B6-Lep(ob/ob) mice. Overexpression of SHP by Ad-SHP decreased blood glucose levels and hepatic gluconeogenic gene expression in B6-Lep(ob/ob) mice. CONCLUSIONS: We have concluded that metformin inhibits hepatic gluconeogenesis through AMPK-dependent regulation of SHP.
A search on AMPK results shows numerous studies on this aspect of metformin activity. The caloric restriction mimetic effects are more theoretical.
QUOTE
Drug Discov Today. 2007 Mar;12(5-6):218-24. Epub 2007 Feb 9.
An anti-aging drug today: from senescence-promoting genes to anti-aging pill.Blagosklonny MV.
Oncotarget Inc., Albany, NY 12203, USA. blagosklonny@oncotarget.com
Numerous mutations increase lifespan in diverse organisms from worms to mammals. Most genes that affect longevity encode components of the target of rapamycin (TOR) pathway, thus revealing potential targets for pharmacological intervention. I propose that one target, TOR itself, stands out, simply because its inhibitor (rapamycin) is a non-toxic, well-tolerated drug that is suitable for everyday oral administration. Preclinical and clinical data indicate that rapamycin is a promising drug for age-related diseases and seems to have anti-tumor, bone-sparing and calorie-restriction-mimicking 'side-effects'. I also discuss other potential anti-aging agents (calorie restriction, metformin, resveratrol and sirtuins) and their targets, interference with the TOR pathway and combination with antioxidants.
An anti-aging drug today: from senescence-promoting genes to anti-aging pill.Blagosklonny MV.
Oncotarget Inc., Albany, NY 12203, USA. blagosklonny@oncotarget.com
Numerous mutations increase lifespan in diverse organisms from worms to mammals. Most genes that affect longevity encode components of the target of rapamycin (TOR) pathway, thus revealing potential targets for pharmacological intervention. I propose that one target, TOR itself, stands out, simply because its inhibitor (rapamycin) is a non-toxic, well-tolerated drug that is suitable for everyday oral administration. Preclinical and clinical data indicate that rapamycin is a promising drug for age-related diseases and seems to have anti-tumor, bone-sparing and calorie-restriction-mimicking 'side-effects'. I also discuss other potential anti-aging agents (calorie restriction, metformin, resveratrol and sirtuins) and their targets, interference with the TOR pathway and combination with antioxidants.
The authors suggestion of using rapamycin for anti-aging effects is interesting also. I would assume that the use of this drug would hinder bodybuilding goals.
Wov, wonderful feedback here.
Benson,
Was it cayenne caps that you had used and liked a lot as a thermogenic? Did you also get any appetite suppression from it?
BTW, the anecdotal evidence from metformin as a weight loss and appetite suppressant is overwhelmingly positive. Many LEF members on VLCD seem to be using it; hence, it appears that -at the very least- people do not appear to be experiencing an increase in cravings as a result. On a more personal note, one of my family members was put on it and even though she continued to eat as before, lost a great deal of weight (as a % of her bodyweight at least)
I a surprised that more people haven't utilized fiber for this purpose btw. Any opinion on fiber caps? For example, would it be potentially beneficial to swallow one or more Psyllium Husk caps with 2-3 glasses of water before the meal? If so how long before the meal? How many?
Finally, I recall using a product called "Satietrol" which I think had potato protein. It was OK; perhaps did have some effect on hunger but was nothing major for me.
Thanks and let's keep them coming
Sub7
Benson,
Was it cayenne caps that you had used and liked a lot as a thermogenic? Did you also get any appetite suppression from it?
BTW, the anecdotal evidence from metformin as a weight loss and appetite suppressant is overwhelmingly positive. Many LEF members on VLCD seem to be using it; hence, it appears that -at the very least- people do not appear to be experiencing an increase in cravings as a result. On a more personal note, one of my family members was put on it and even though she continued to eat as before, lost a great deal of weight (as a % of her bodyweight at least)
I a surprised that more people haven't utilized fiber for this purpose btw. Any opinion on fiber caps? For example, would it be potentially beneficial to swallow one or more Psyllium Husk caps with 2-3 glasses of water before the meal? If so how long before the meal? How many?
Finally, I recall using a product called "Satietrol" which I think had potato protein. It was OK; perhaps did have some effect on hunger but was nothing major for me.
Thanks and let's keep them coming
Sub7
Psuedo Ephedrine if I recall correctly is kept behind the counter and is rather expensive no? I went and bought some on Bensons advice a year or so ago, but it contained other actives and I think I ended up getting sick and using it for that.
Nicotine gum would be great, but its also hella expensive, plus I'd rather dip.
Psyllium Husk caps sound like a good idea, I've really been wanting to increase my fiber intake and this would seem like a good hunger control device as well.
Nicotine gum would be great, but its also hella expensive, plus I'd rather dip.
Psyllium Husk caps sound like a good idea, I've really been wanting to increase my fiber intake and this would seem like a good hunger control device as well.
QUOTE(Sub7 @ Feb 25 2008, 02:40 PM) [snapback]460964[/snapback]
Benson,
Was it cayenne caps that you had used and liked a lot as a thermogenic? Did you also get any appetite suppression from it?
Was it cayenne caps that you had used and liked a lot as a thermogenic? Did you also get any appetite suppression from it?
Yes. Very thermogenic but nothing special in terms of appetite suppression IIRC.
Re: pseudoephedrine, it is now 'behind the counter' as a result of the meth control act but its not expensive, especially if you go with the house brand and its available with nothing else in tow.
QUOTE(Sub7 @ Feb 25 2008, 01:40 PM) [snapback]460964[/snapback]
Wov, wonderful feedback here.
Benson,
Was it cayenne caps that you had used and liked a lot as a thermogenic? Did you also get any appetite suppression from it?
BTW, the anecdotal evidence from metformin as a weight loss and appetite suppressant is overwhelmingly positive. Many LEF members on VLCD seem to be using it; hence, it appears that -at the very least- people do not appear to be experiencing an increase in cravings as a result. On a more personal note, one of my family members was put on it and even though she continued to eat as before, lost a great deal of weight (as a % of her bodyweight at least)
I a surprised that more people haven't utilized fiber for this purpose btw. Any opinion on fiber caps? For example, would it be potentially beneficial to swallow one or more Psyllium Husk caps with 2-3 glasses of water before the meal? If so how long before the meal? How many?
Finally, I recall using a product called "Satietrol" which I think had potato protein. It was OK; perhaps did have some effect on hunger but was nothing major for me.
Thanks and let's keep them coming
Sub7
Benson,
Was it cayenne caps that you had used and liked a lot as a thermogenic? Did you also get any appetite suppression from it?
BTW, the anecdotal evidence from metformin as a weight loss and appetite suppressant is overwhelmingly positive. Many LEF members on VLCD seem to be using it; hence, it appears that -at the very least- people do not appear to be experiencing an increase in cravings as a result. On a more personal note, one of my family members was put on it and even though she continued to eat as before, lost a great deal of weight (as a % of her bodyweight at least)
I a surprised that more people haven't utilized fiber for this purpose btw. Any opinion on fiber caps? For example, would it be potentially beneficial to swallow one or more Psyllium Husk caps with 2-3 glasses of water before the meal? If so how long before the meal? How many?
Finally, I recall using a product called "Satietrol" which I think had potato protein. It was OK; perhaps did have some effect on hunger but was nothing major for me.
Thanks and let's keep them coming
Sub7
I prefer fiber one from a cost/fiber basis.
Benson how many mg's are we shooting for with the PE? And only once daily correct? Being poor has handled my appetite nicely more recently, but I'm under the assumption my new job will eventually pay me and having some appetite control methods other than poverty would be nice lol
For myself, nicotine gum + meridia + caffeine are an unbeatable combination.
The stack does increase my heart rate significantly however.
The stack does increase my heart rate significantly however.
I would not touch any of the afore mentioned substances with a 6 foot pole(unless you are morbidly obese which non of you are). as spook said, body composition is a marathon, not a sprint.
In the last year, all my clients who are dieting received non of this crap and the results are very good.
In the last year, all my clients who are dieting received non of this crap and the results are very good.
Picked up some pseudophed 12 hour from Target yesterday. Its the only active in the pill. Don't remember the price, I think it was $6ish. I took one yesterday around noon and didn't even want dinner last night. So far so good. I'll keep a few pieces of nicotine gum on me today in case the cravings get worse and see how that helps.
QUOTE
Many LEF members on VLCD
I know Life Extension but what is VLCD??
very low cal diet. but some people use the acronym for low carb as well.
QUOTE(D-termine @ Feb 26 2008, 12:18 AM) [snapback]461152[/snapback]
Benson how many mg's are we shooting for with the PE? And only once daily correct? Being poor has handled my appetite nicely more recently, but I'm under the assumption my new job will eventually pay me and having some appetite control methods other than poverty would be nice lol
I think the 12h formulation is 120mg/tablet. Take in the AM.
There is also a 240mg 24h formula but as I have said, for me anyway it seems to have a direct effect on the colon where it is still dissolving a day later and binds me up completely.
Some have speculated that neutralizing some stomach acid may help reduce hunger and cravings and have suggested things like TAGAMET for this purpose (http://www.rxlist.com/cgi/generic/cimet.htm)
Anyone have any experience with this? Any suggestions as to why and how less stomach acid = less hunger?
Thanks to all
Anyone have any experience with this? Any suggestions as to why and how less stomach acid = less hunger?
Thanks to all
QUOTE(Sub7 @ Mar 1 2008, 07:42 PM) [snapback]462603[/snapback]
Some have speculated that neutralizing some stomach acid may help reduce hunger and cravings and have suggested things like TAGAMET for this purpose
Cimetidine is great for growing boobs
QUOTE(Sub7 @ Mar 1 2008, 04:42 PM) [snapback]462603[/snapback]
Some have speculated that neutralizing some stomach acid may help reduce hunger and cravings and have suggested things like TAGAMET for this purpose (http://www.rxlist.com/cgi/generic/cimet.htm)
Anyone have any experience with this? Any suggestions as to why and how less stomach acid = less hunger?
Thanks to all
Anyone have any experience with this? Any suggestions as to why and how less stomach acid = less hunger?
Thanks to all
I remember reading some studies on this. I think I tried Ranitidine at the time to see if it worked and didn't get anything noticable from it. Need to look at the research again.
Acta Physiol Scand. 1997 Apr;159(4):321-5.
Effect of cimetidine on basal and postprandial plasma concentrations of cholecystokinin and gastrin in humans.
Sta-Birketvedt G, Waldum HL, Vonen B, Florholmen J.
Laboratory of Gastroenterology, University of Troms, Norway.
Cimetidine reduces the appetite and weight in healthy overweight subjects. Gastrointestinal regulatory peptides such as cholecystokinin (CCK) have been proposed to mediate the satiety signal from gut to brain. Therefore, the effect of cimetidine on basal and postprandial plasma concentrations of cholecystokinin and gastrin was studied. After an overnight fast, 12 healthy volunteers were given cimetidine (400 mg) on day 1, breakfast on day 2, and cimetidine 20 min before breakfast on day 3. Plasma concentrations of cholecystokinin and gastrin were measured by radioimmunoassay. Plasma cholecystokinin concentration increased with one major peak observed 30 min and one smaller peak observed 120 min after intake of cimetidine. The meal induced an increase in the plasma concentration of cholecystokinin, while cimetidine prior to the meal elicited a sustained postprandial cholecystokinin response. Cimetidine had no effect on the basal plasma concentration of gastrin. The meal induced an increase in the plasma concentration of gastrin, while cimetidine prior to the meal elicited a sustained postprandial gastrin response. In conclusion, cimetidine increases the basal concentration of plasma cholecystokinin and elicits a sustained postprandial response of both cholecystokinin and gastrin. At least the cholecystokinin response may be one mechanism by which cimetidine reduces the appetite.
Int J Obes Relat Metab Disord. 1998 Nov;22(11):1041-5.
Comment in:
Int J Obes Relat Metab Disord. 1999 May;23(5):550-1.
Cimetidine reduces weight and improves metabolic control in overweight patients with type 2 diabetes.
Sta-Birketvedt G, Paus PN, Ganss R, Ingebretsen OC, Florholmen J.
Laboratory of Gastroenterology, University of Troms, Norway.
OBJECTIVE: To investigate the weight-reducing effect of cimetidine in overweight patients with Type 2 diabetes. DESIGN: A 12-week clinical intervention study of 400 mg cimetidine prescribed three times daily in a randomised, double-blind, placebo-controlled design. SUBJECTS: Forty-three overweight patients with Type 2 diabetes (age 18-65 y, body mass index (BMI) 27.2-48.2 kg/m2). MEASUREMENTS: Body weight, BMI, body fat, waist and hip circumference, waist/hip ratio, blood pressure, fasting blood glucose, HbA1c, plasma concentrations of insulin, insulin/glucose ratio and lipids at the start and after 12 weeks, and daily recordings of appetite. RESULTS: Subjects given cimetidine (n = 19) and placebo (n = 24) lost 5.0 +/- 2.2 kg (mean +/- s.d.) and 1.3 +/- 1.1 kg, respectively. Significant reductions were observed in appetite, body fat (29.9 +/- 6.6% to 25.3 +/- 7.4%), waist circumference (111.5 +/- 10.3 cm to 107.4 +/- 10.6 cm), waist/hip ratio (0.96 +/- 0.08 to 0.94 +/- 0.08), and systolic and diastolic blood pressure (reductions of 6.9 +/- 11.4 mm Hg and 6.0 +/- 6.6 mm Hg, respectively) in cimetidine group only. Significant decreases in fasting concentrations of blood glucose, HbA1c, plasma insulin, insulin/glucose ratio, plasma triglycerides and a significant increase in plasma high-density lipoprotein cholesterol were observed in the cimetidine group only. CONCLUSIONS: Cimetidine reduces appetite and body weight, and improves metabolic control in overweight subjects with Type 2 diabetes.
Effect of cimetidine on basal and postprandial plasma concentrations of cholecystokinin and gastrin in humans.
Sta-Birketvedt G, Waldum HL, Vonen B, Florholmen J.
Laboratory of Gastroenterology, University of Troms, Norway.
Cimetidine reduces the appetite and weight in healthy overweight subjects. Gastrointestinal regulatory peptides such as cholecystokinin (CCK) have been proposed to mediate the satiety signal from gut to brain. Therefore, the effect of cimetidine on basal and postprandial plasma concentrations of cholecystokinin and gastrin was studied. After an overnight fast, 12 healthy volunteers were given cimetidine (400 mg) on day 1, breakfast on day 2, and cimetidine 20 min before breakfast on day 3. Plasma concentrations of cholecystokinin and gastrin were measured by radioimmunoassay. Plasma cholecystokinin concentration increased with one major peak observed 30 min and one smaller peak observed 120 min after intake of cimetidine. The meal induced an increase in the plasma concentration of cholecystokinin, while cimetidine prior to the meal elicited a sustained postprandial cholecystokinin response. Cimetidine had no effect on the basal plasma concentration of gastrin. The meal induced an increase in the plasma concentration of gastrin, while cimetidine prior to the meal elicited a sustained postprandial gastrin response. In conclusion, cimetidine increases the basal concentration of plasma cholecystokinin and elicits a sustained postprandial response of both cholecystokinin and gastrin. At least the cholecystokinin response may be one mechanism by which cimetidine reduces the appetite.
Int J Obes Relat Metab Disord. 1998 Nov;22(11):1041-5.
Comment in:
Int J Obes Relat Metab Disord. 1999 May;23(5):550-1.
Cimetidine reduces weight and improves metabolic control in overweight patients with type 2 diabetes.
Sta-Birketvedt G, Paus PN, Ganss R, Ingebretsen OC, Florholmen J.
Laboratory of Gastroenterology, University of Troms, Norway.
OBJECTIVE: To investigate the weight-reducing effect of cimetidine in overweight patients with Type 2 diabetes. DESIGN: A 12-week clinical intervention study of 400 mg cimetidine prescribed three times daily in a randomised, double-blind, placebo-controlled design. SUBJECTS: Forty-three overweight patients with Type 2 diabetes (age 18-65 y, body mass index (BMI) 27.2-48.2 kg/m2). MEASUREMENTS: Body weight, BMI, body fat, waist and hip circumference, waist/hip ratio, blood pressure, fasting blood glucose, HbA1c, plasma concentrations of insulin, insulin/glucose ratio and lipids at the start and after 12 weeks, and daily recordings of appetite. RESULTS: Subjects given cimetidine (n = 19) and placebo (n = 24) lost 5.0 +/- 2.2 kg (mean +/- s.d.) and 1.3 +/- 1.1 kg, respectively. Significant reductions were observed in appetite, body fat (29.9 +/- 6.6% to 25.3 +/- 7.4%), waist circumference (111.5 +/- 10.3 cm to 107.4 +/- 10.6 cm), waist/hip ratio (0.96 +/- 0.08 to 0.94 +/- 0.08), and systolic and diastolic blood pressure (reductions of 6.9 +/- 11.4 mm Hg and 6.0 +/- 6.6 mm Hg, respectively) in cimetidine group only. Significant decreases in fasting concentrations of blood glucose, HbA1c, plasma insulin, insulin/glucose ratio, plasma triglycerides and a significant increase in plasma high-density lipoprotein cholesterol were observed in the cimetidine group only. CONCLUSIONS: Cimetidine reduces appetite and body weight, and improves metabolic control in overweight subjects with Type 2 diabetes.
Would other methods reducing the stomach's acidity lso have hunger suppressing effects? Proton pumps for example...?
QUOTE(Sub7 @ Mar 2 2008, 08:13 PM) [snapback]462918[/snapback]
Would other methods reducing the stomach's acidity lso have hunger suppressing effects? Proton pumps for example...?
One study I looked at says no. They looked at H2 antagonists like cimetidine and famotidine along with a proton pump inhibitor (omeprazole) and saw no benefit from the omeprazole. They speculate that reduced acidity is not the reason for the appetite reduction from H2 antagonists.
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