Energy balance: role of genetics and activity

It is clear from the above discussion that much remains to be learned about both energy intake and energy expenditure. Obesity in humans is not likely to be caused by one gene, as it is in certain rodent models of obesity, such as the ob/ob mouse and the fa/fa rat. It is likely to be a polygenic condition in which numerous genes interact with each other and the environment to express the obesity phenotype. It is likely that genes that affect energy intake as well as genes that affect energy expenditure are involved. The role of leptin as a putative factor in signaling the extent of the fat mass to the central nervous system and controlling both food intake and energy expenditure is unclear at this time. The genetics of energy expenditure are also not clear at this time. There are mechanisms of nutrient partitioning, such as respiratory quotient and lipoprotein lipase activity, that are being discovered to be important. In addition, insulin sensitivity is likely to play a role in the etiology of obesity. Much more investigation will be required before we have a clearer picture of how the above-named factors interact, what the genetic contribution to this is, and how important each factor is to the overall phenotypic expression of obesity.