Conclusions

Abstract

It has generally been assumed that appetite is regulated by a homeostatic system that serves to maintain energy balance. Accordingly, attempts to identify the physiological mechanisms underlying this homeostasis have dominated research in the area, and experimental models of obesity have been studied mainly for their potential to provide insight into these mechanisms. Contemporary reviews of the control of food intake may therefore present extensive and sophisticated models which imply multiple and sensitive mechanisms for homeostatic regulation (e.g., Bray, 1989; Weigle, 1994), akin to those established for ensuring sodium balance. Arguably, though, much of this has been of little direct relevance to understanding variance in human obesity, which appears not to be readily explained by obvious defects in any part of the many physiological or biomolecular systems examined to date.