Insulin is the mediator of feecling‐related thermogenesis: insulin resistance and/or deficiency results in a thermogenic defect which contributes to the pathogenesis of obesity

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Abstract
Obesity is characterized by insulin resistance which predisposes to the development of impaired glucose tolerance. It is postulated that in addition to its role in carbohydrate metabolism, insulin is the mediator of feeding-related increases in thermogenesis (the thermic effect of food and dietary-induced thermogenesis). The development of insulin resistance and/or deficiency is postulated to result in a decrease in feeding-related, insulin-mediated thermogenesis. As a consequence of this thermogenic defect there is an increase in efficiency of weight gain which accelerates the development and facilitates the maintenance of the obese state. Abnormalities in the insulin axis are thus not only involved in the pathogenesis of the carbohydrate intolerance of obesity but are also proposed as having a central role in a dysregulation of energy balance which contributes to the pathogenesis of obesity.