A positive energy balance is known to cause insulin resistance. Although the reasons underlying this disorder are rather complex, they are likely related to ectopic fat deposition (fat deposition in nonadipose tissue). This study tested the hypothesis that the body’s failure to expand the subcutaneous adipose tissue depot might be one key mechanism responsible for insulin resistance and beta-cell failure. The study authors sought to explore whether a modest overexpression of adiponectin in obese mice (Ad Tg ob/ob) had an impact on metabolic variables. Their findings showed that glucose, insulin, triglyceride, and free fatty acids levels improved in these mice compared to ob/ob mice. The obese mice that overexpressed adiponectin also had lower macrophage infiltration of adipose tissue and systemic inflammation (circulating interleukin-6 levels and tumour necrosis factor-a in adipose tissue). These transgenic mice were morbidly obese, with more adipose tissue than ob/ob mice, although they had a better metabolic profile. This data suggests that adiponectin acts as a peripheral “starvation” signal to promote the storage of energy (triglycerides) in adipose tissue, with reduced triglycerides in the liver and skeletal muscle. This may help explain why obese mice with high levels of adiponectin have improved systemic insulin sensitivity. These obese mice that overexpress adiponectin form a new model of morbid obesity, one that is associated with an improved metabolic profile.
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