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Cortisol regeneration by increased 11beta-HSD-1.
Interconversion of inactive cortisone to active cortisol.


J Nutr. 2007 Dec;137(12):2616-21.

Sucrose access differentially modifies 11beta-hydroxysteroid dehydrogenase-1 and hexose-6-phosphate dehydrogenase message in liver and adipose tissue in rats.

London E, Lala G, Berger R, Panzenbeck A, Kohli AA, Renner M, Jackson A, Raynor T, Loya K, Castonguay TW.

Department of Nutrition and Food Science, University of Maryland, College Park, MD 20742, USA.

11Beta-hydroxysteroid dehydrogenase-1 (11beta-HSD-1) plays a key role in the regulation of intracellular glucocorticoid concentrations. Increased message and/or activity of adipose 11beta-HSD-1 are characteristics of human and animal models of obesity. Hexose-6-phosphate dehydrogenase (H6PDH) is colocalized with 11beta-HSD-1 and may be a critical factor in determining the oxo-reductase activity of 11beta-HSD-1. This study examined the effects of sucrose solution access on body weight, body composition, and message of 11beta-HSD-1 and H6PDH in mesenteric adipose and liver. Rats were assigned to 3 groups: 1) control (ad libitum intake of nonpurified diet and water only); 2) ad libitum intake of 16% sucrose solution (S16); or 3) ad libitum intake of 32% sucrose solution (S32) in addition to ad libitum intake of diet and water. The S32 group consumed more energy daily than the S16 and control groups, yet body weight did not differ among groups. Percentages of body fat did not differ between the S16 and S32 groups but were higher than in controls. Hepatic 11beta-HSD-1 message was suppressed by 46% in the S16 group and by 47% in the S32 group, whereas the H6PDH message nearly doubled in the S16 group compared to the control group. In mesenteric fat, 11beta-HSD-1 message increased 23-fold in the S16 group and 32-fold in the S32 group and the H6PDH message increased 3.5-fold in the S16 group compared to the control group. These data demonstrate that sucrose can promote increased 11beta-HSD-1 and H6PDH message in mesenteric fat while concomitantly decreasing 11beta-HSD-1 message and increasing H6PDH message in liver. These observations support the hypothesis that sucrose access causes obesity via its ability to increase adipose 11beta-HSD-1.



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Your interpretation of this abstract is wrong.

how so?

What that abstract said was there is a shift in fat from liver to intestinal area.

By that shift, the abstract concluded that the mechanism of action involved in fat distribution is 11beta-HSD1.

Thia has nothting to do with "evils" of sugar.

Any hypercaloric diet would be bad.

more evil than ben laden.

are you still stuck in your "calorie is a calorie" bubble?

You have quoted 23x increase and 32x increase 11 beta-HSD, to show the evil of sugar. There are many problems with that statement

(1) you don't know what the normal response of 11beta-HSD1 is in the mesenteric fat in the presence of excess energy. It may very well be, when excess calories are consumed, 11beta NORMALLY increases 30 fold.

(2) In the experiment, there is no control variable with regard to the TYPE of food consumed. For example, the experiment doesn't compare how much 11B-HSD increases in mesenteric area when excess FAT is consumed. The reason why there is no control variable with respect to the TYPE of macronutrient is because "evil" of sugar was not what the experiment was designed to show.

(3) When a certain area of human body stores more fat than others, to shift fat away from one area and to store it in another, the shift in 11beta HSD will not be equal in both liver and intestinal area. Thus, 30x increase in 11B-HSD may very well be needed to shift the fat from liver, where 11B-HSD was DECREASED by 50%. This might be a normal response.

(4) The amount of fat accumulation is directly a function of the excess energy. Thus, the presence of 11betaHSD doesn't magically create fat.

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Basically, that abstract had nothing to do with evils of sugar.

When you read an abstract, you need to understand what the experiment was designed to show.

liorrh:

Just to add one more point, you understand that cortisol/cortisone is not "evil," right?

It is necessary for an effective energy expenditure.

I will try to explain this in Inner Circle.

Here would be fine as well

lol.

Cortisol's main role is to deploy energy in sufficient quantities in different situations (the amount being proportionate to the level of stress that a situation presents). Understandably, we cannot live without cortisol. Any attempt to systemically lower cortisol too much will lead to decrease in energy expenditure, not to mention potential illness and eventually to death.

Considering that cortisol is "designed" to cope with stress, increases in cortisol production will exact energy deployment from all tissues. Necessarily, it will promote catabolism (e.g., proteolysis), glycolysis (use of stored glycogen), and lipolysis. In longer term, it has a "negative" effect -- it preferentially restores visceral fat at the expense of restoring other tissues. (In other words, it rechannels energy toward storage). This makes sense, in that, should the stressful situation be encountered again, energy can be most efficiently deployed from fat cells.

Under normal circumstances, however, cortisol's negative effect is neutralized by the presence of other hormones.

To understand this, consider exercising daily. When one exercises, cortisol release is increased, to promote greater energy deployment. But, strangely, extra cortisol released during exercise doesn't cause a body to accumulate visceral fat. The reason is that other hormones neutralize cortisol in proper tissues. For instance, GH released during/after exercise blocks 11B-HSD1.

In another example, consider caloric restriction. When one decreases calories, there is increase in cortisol. However, caloric restriction PROLONGS life. Why? Becaise. again, there are more than just corsiol involved. When one fasts, there is increased GH release, which, again, neutralizes/blocks cortisol.

As one ages, the balance between cortisol and other hormones changes. For example, GH level decreases as one gets older, and therefore, GH/cortisol ratio becomes smaller. This is evidenced by the fact that older men tend to accumulate belly fat. In contrast to young men (below age of 30), in the presence of stress, older men will quickly develop stress-related illnes or disease.

In summary, one cannot just try to eliminate cortisol -- it is necessary for one's body.

Ideally, what one would like is to change cortisol/other hormone balance that promotes favorable body composition, while maintaining proper cortisol level.