An elaborate network of central and peripheral neurohormonal signals has evolved to regulate feeding, one of the primal activities necessary for survival and self-preservation. Despite decades of animal and human research, the full extent of the processes and humors involved in the regulation of food intake remains to be elucidated. Current understanding indicates that energy homeostasis in health is predicated upon a balance between orexigenic and anorexigenic factors, both centrally and peripherally. Virtually all of the peripheral signals (e.g., insulin, PYY, leptin, CCK) are triggered by food ingestion and attenuated by fasting or starvation, indicating a response system that is tailored at satiety and meal termination. Ghrelin, the only peripheral signal activated preprandially, may be unique in its role as a rare peripheral signal for hunger and meal initiation.

The rarity of peripheral hormonal signals that trigger meal initiation may be a reflection of the incompleteness of current understanding. However, a more plausible explanation is that appetite and hunger are under predominantly central control, and are orchestrated by neuronal projections from various brain centers to the NPY-expression arcuate neurons. The central control of feeding is organized into an integrated neuroendocrine system that either stimulates or inhibits food intake. The orexigenic (e.g., NPY, AgRP) and anorexigenic (e.g., melanocortins) components of this system receive afferent neuroendocrine and metabolic signals from the periphery but may also be subject to local and paracrine influences, as well as inputs from higher brain centers. The coordinate regulation of these various opposing mechanisms leads to energy homeostasis that is physiologically skewed toward positive balance. An increased understanding of these mechanisms is a prerequisite for the discovery of drug interventions that can dependably modulate food intake and prevent or treat obesity.

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