The case for obesity per se being a major cause of insulin resistance has been made. There is evidence that each of the control points of insulin on glucose metabolism are negatively influenced by lipid oversupply, a characteristic of the obese state. The answer to the corollary, whether insulin resistance (a universal concomitant of obesity) can in turn lead to obesity via a decrease in thermogenesis, is more complex. Overall, the answer would appear to be no. On a population basis, obese individuals would not appear to have lower metabolic rates, whether expressed on a lean tissue or any other basis, than lean individuals. Even in the subpopulation of hypometabolic obese, there are no convincing data that the reduced metabolic rate is linked to particularly severe insulin resistance. Further, improving insulin action by weight loss would not appear to increase thermogenesis as would be predicted if insulin resistance impaired thermogenesis. A case can be made for reductions in a specific aspect of energy expenditure in obesity, that of meal-induced or glucose-induced thermogenesis, and this may be due to insulin resistance. However, meal-induced thermogenesis is a small component of total energy expenditure and total energy expenditure is not different between lean and obese. That leaves the intriguing possibility that a relative failure of prandial thermogenesis has an impact upon energy balance via impairment of satiety (related to reduced metabolic flux) and thus by increasing intake. While a potentially fruitful research avenue, too few data exist on this possibility for it to be anything more than speculative at this stage.