ABSTRACT
From a thermodynamic point of view, obesity can, in essence, be considered the result of a positive imbalance between food intake and energy expenditure, with the resultant excess energy accumulating as fat in the adipose tissue. Although outwardly this energy balance equation may appear simple, it can be modulated by many other factors, particularly the preferential partitioning of energy toward specific tissues and organs. In
fact, it could be argued that some individuals may have an enhanced capacity to extract energy from blood into the adipose tissue, thus facilitating fat deposition. Conversely, individuals that preferentially partition fuel into lean and/or oxidative tissues may facilitate energy dissipation. It is still unclear whether defects in the mechanism of fuel partitioning are important causes of human obesity; however, recently reported genetically modified animal models have provided support for this concept as a potential strategy for treatment of obesity and its protean complications.
