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• _4 wasQuotedFrom 16020439 provenance.
• _4 value "Although the exact mechanism of resistin function has yet to be identified, Steppan et al. (100) observed increased circulating resistin levels in diet-induced and genetic models of obesity. Inhibition of resistin in these models restored insulin action, whereas administration of resistin inhibited insulin action in control animals. Surprisingly, the evidence linking resistin to diabetes and obesity in humans is less clear. Serum content of resistin is unaffected by obesity and insulin resistance in humans (37). Lee et al. (66) compared BMI, fat mass, and insulin action to resistin levels in 243 subjects (male and female) and observed no relationship. There was also no difference in resistin between lean and obese insulin-resistant subjects. Serum resistin can be elevated in Type 2 diabetes patients, but there was no relationship between adiposity and insulin (70), whereas others have reported no difference in obese, obese diabetic, and nonobese subjects (37). Although there are conflicting reports as to the relationship of resistin to adiposity (5), most investigations agree that resistin is not related to insulin resistance (107). To date, there is no information on the interaction between exercise and resistin. Because the role of resistin in regulating insulin action is unclear at this time, there appears to be little rationale to investigate the influence of exercise on this particular adipocytokine. Interleukin (IL-6). IL-6 is a multifunctional cytokine secreted by numerous cell types including immune cells, skeletal muscle, and adipose tissue. In an effort to determine function, Kim et al. (58) pretreated mice with IL-6 before a hyperinsulinemic- euglycemic clamp. IL-6 blunted skeletal muscle glucose disposal as well as IRS-1-associated phosphatidylinositol 3-kinase activity (58)." provenance.