Human obesity: a defect in lipid oxidation or in thermogenesis?

Numerous animal studies have shown that the development of obesity can depend on a decreased sympathetic nervous system activity but it has not been possible to convincingly demonstrate in humans that an excessive accumulation of adipose tissue might also be attributable to this factor. However, results from recent studies suggest that the contribution of the sympathetic nervous system to the development of human obesity may be greater than that generally believed by the scientific community. Indeed, experimental data show that the decrease in lipid oxidation induced by beta adrenergic blockade under free living conditions is substantially higher than the decrease in energy expenditure. Moreover, there are individual variations in the relative capacity to use lipid as an energy substrate under standardized conditions of diet composition. If the contribution of lipid to daily energy expenditure is reduced, there are two options to reach energy balance if physical activity habits are not modified. The first possibility is reduction in the relative lipid content of the diet to match the lipid content of the fuel mix oxidized. The second option is a gain in body weight and fat until the associated increase in the lipid content of the substrate mix is sufficient to re-equilibrate substrate and energy balance. Under high fat diet conditions, this gain in body weight and fat can be large enough to lead to an obese state. As described in this report, an integration of these observations suggests that further research pertaining to the role of sympathetic nervous system activity in human obesity should be focused as much on lipid oxidation as on thermogenesis.