Conclusions

In recent years there has been an intense focus on abnormalities of FFA metabolism in the pathophysiology of insulin resistance, its metabolic complications, and type 2 diabetes. In fact, because abnormalities of FFA metabolism can often be detected well in advance of abnormalities of glucose and carbohydrate metabolism, some have postulated that these abnormalities are a fundamental cause of type 2 diabetes. FFAs likely play an important role in communication between organs, and signal the body's energy status to the hypothalamus. Based on the belief that elevated FFAs are both diabetogenic and proatherogenic, attempts have been made to develop specific pharmacotherapies to lower plasma FFA concentrations. We postulate that elevated plasma FFA concentration (and its downstream deleterious effects) is but one consequence of the fundamental cause of insulin resistance and type 2 diabetes, i.e., positive net energy balance and obesity that develop as a consequence of an imbalance between calorie consumption and energy expenditure, modulated at multiple levels by the genetic makeup of the individual. In fact we predict that therapies directed solely at reducing plasma FFA concentration, if they do not address the factors responsible for the positive net energy balance, are doomed to fail or could result in unintended deleterious consequences.

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