Regulation of body weight.

REGULATION OF BODY WEIGHT is a complex and dynamic process. Many aspects of this regulation have been addressed by recent publications in the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. Among them are delineation of pathways signaling satiation; interactions with other physiological control systems, notably cardiovascular and reproductive systems; exploration of factors that determine susceptibility to diet-induced obesity; and temporal aspects of body weight regulation. The last includes rhythmic events of various cycle lengths, from infradian to circa-annual periods, and also developmental and age-related events. Today, leptin, neuropeptide Y (NPY), orexins, cocaine and amphetamine-regulated transcript (CART), amylin, and proopiomelanocortin (POMC) are studied largely in relation to their putative or demonstrated roles in the regulation of food intake and of body weight. Recent studies published in the journal illustrate that most, if not all, of these peptides are also involved in regulation of other behavioral or biochemical processes. Thus orexins A and B given intrathe-cally are shown to activate sympathetic preganglionic neurons and raise both blood pressure and heart rate (3). Similar effects are seen after central orexin injections that target sites in the medulla known to be involved in cardiovascular control (7). The effect of intracerebroventricular CART to reduce food intake occurs primarily at a hindbrain site and is associated with specific alterations of motor behavior that appear unrelated to ingestion (1). Amylin, infused into the nucleus accumbens, reduces not only feeding and drinking but also ambulation (4). Administration of NPY intracerebroventricularly stimulates feeding and also inhibits sexual behavior in male rats (2) and in female hamsters (10). The latter report shows that the feeding and sexual behavior responses are mediated by different receptor subtypes. Injection of leptin intra-cerebroventricularly reduces food intake and, as expected , this effect is attenuated by SHU9119, an antagonist of melanocortin receptors. The same leptin injection also elevates circulating gonadotropin levels and increases the weight of seminal vesicle; these effects were not affected by SHU9119, suggesting that leptin affects the two systems via separable circuits (22). Other interactions between the reproductive system and regulation of body weight are also addressed. In female rats, estradiol reduces meal size, food intake, and body weight largely by increasing the potency of satiation signals such as glucagon (18). In the nucleus of the solitary tract and downstream sites involved in negative feedback control of meal size, estradiol enhances the induction of c-Fos by feeding (16). Typically such studies …