Not sure where i seen it posted but somewhere today on the forums i seen a post asking for factors that influence insulin resistance

Hope this helps

Not sure of the exact title of this reference it is from a paper I received from Dan Moore:

Excerpts:

"The interaction between overweight and insulin resistance is complex and involves
several epidemiological associations (figure 1). Briefly reviewed, these are:

- Fat distribution: Patients with central adiposity have higher insulin levels and
are more insulin resistant than subjects with similar weight but with a
peripheral type of obesity (22-24).

- Plasma FFA levels: The extent of (direct) exposure of liver and muscle cells
to FFA concentrations might be involved in mediating tissue specific insulin
resistance. For instance, experimental elevation of FFA induces insulin
resistance (25-27). At the cellular level, FFA and their metabolic products can
reduce insulin signalling in muscle and liver (27).

- Ectopic triglyceride accumulation: TG content of skeletal muscle and liver
correlates directly with insulin resistance (27-31). These observations suggest
that accumulation of fat in liver and muscle tissue might (partly) mediate
obesity-induced insulin resistance.

- Adipokines: Another major mechanism linking obesity to insulin resistance is
a group of peptides, made by fat cells that alter insulin sensitivity. Adiponectin
has been shown to reduce insulin resistance and reduced levels of
adiponectin are found in progressive obesity (32;33). Tumor necrosis factoralpha
(TNF��), interleukin-6, resistin and leptin increase insulin resistance
(34). Elevated levels of these adipocytokines are observed with obesity
(34;35). Various adipose tissue beds produce different amounts of these
peptides, perhaps adding to the regional differences in the contribution of
these adipose depots to insulin resistance.

- Hyperglycaemia: Hyperglycaemia itself is known to induce insulin resistance
(36). This partially reversible phenomenon is known as glucose toxicity. In
cells, oxidative glucose metabolism will always lead to production of reactive
oxygen species, normally detoxified by catalase and superoxide dismutase.
Because these enzymes are present in low amounts in ��-cells,
hyperglycaemia can result in the production of large amounts of reactive
oxygen species in ��-cells, with subsequent damage to cellular components.

- Number of insulin receptors, post-receptor signalling by insulin and synthesis
and translocation of GLUT4: It is suspected that alterations in de expression
and/or function of these factors underlie insulin resistance in obesity as well
as in type II diabetes. Among the many molecules involved in the intracellular
processing of the signal provided by insulin, insulin receptor substrate (IRS)-
2, the protein kinase B (PKB)-beta isoform and the forkhead transcription
factor Foxo1a (FKHR) are of particular interest in this context as recent data
have provided strong evidence that dysfunction of these proteins results in
insulin resistance in vivo (37;38).

- Glucoregulatory hormones: Glucocorticoids (39), sex steroids (40), growth
hormone (41), and catecholamines (42;43) influence tissue insulin sensitivity.

- Oxidative stress and vascular reactivity: These factors have also been
suggested to be involved in the development of insulin resistance (44-46).
However, oxidative stress, vascular reactivity, inflammation and insulin
resistance seem to be interrelated and more research is needed to elucidate
this relationship.

- Diurnal rhythms: It is recently shown in healthy humans that insulin sensitivity
changes rhythmically during the day (47)."

thanks
Coach Hale
www.maxcondition.com