The incidence of obesity and other eating disorders continues to climb worldwide. Eating is controlled by a plethora of factors; most importantly peripheral gastrointestinal hormones that act directly or indirectly on the central nervous system play amajor role. The increase in the incidence of obesity seems to be largely due to increased energy intake, combined with a reduction in energy expenditure. For larger animals (including humans), it seems to be easier to influence overall energy balance via a control of energy intake rather than energy expenditure (the situation may be opposite in small animals, e.g., mice). Hence, we must understand controls of eating to understand their potential contribution to the development of obesity. It is generally accepted that factors that influence food intake and consequently body fat are conceptualized as those that influence when individuals start eating and those that influence when eating, once begun, will end; i.e., factors that stimulate appetite or eating per se and those that stimulate fullness or satiation. Except in rare circumstances, eating is not initiated by physiological factors associated with energy needs but by factors such as habit, time of day, the social situation, food availability, and so on. The amount eaten (i.e., meal size), on the other hand, is determined by satiation factors generated by the gastrointestinal system interacting with ingested food. The best known satiation factor is the intestinal peptide, cholecystokinin (CCK).Satiation factors interact in the brain with signals emanating from adipose tissue and other organs indicating how lean or fat the individual is. These adiposity signals, such as leptin and insulin, signal the amount of adipose tissue to the brain and interact with receptors in the hypothalamus; they have potent effects on food intake and energy expenditure. It is important to realize, though, that both groups of signals interact, and that the concentrations of the adiposity signals insulin and leptin also fluctuate in relation to food intake. Apart from the distinction of short-term meal-associated signals versus long-term adiposity signals, eating controls can be classified into homeostatic controls of eating versus hedonic controls; the latter influence reward driven processes. Such processes, which are also influenced by gastrointestinal hormones, can overcome the homeostatic controls of eating under certain conditions. Finally, sex differences in the incidence and in particular the extent of obesity may depend on estrogen's modulation of eating controls.
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