Classically, the hypothalamus has been considered a grouping of regulatory centers governing homeostasis. With respect to eating, the ventromedial nucleus of the hypothalamus serves as a satiety center and the lateral hypo-thalamic area serves as a feeding center. Together, these areas coordinate the processes that govern eating behavior and the subjective perception of satiety. These hypothalamic areas also influence the secretion of hormones, partic-
Dorsal hypothalamic area
Paraventricular nucleus Anterior hypothalamic area
Portal hypophyseal vessel
Posterior hypothalamic nucleus
Ventromedial nucleus Premammillary nucleus Medial mammillary nucleus Lateral mammillary nucleus Mammillary body
^mGUQER^fe The hypothalamus and its nuclei. The connections between the hypothalamus and the pituitary gland are also shown. (Modified from Ganong WF.
Lesions in the ventromedial nucleus in experimental animals lead to morbid obesity as a result of unrestricted eating (hyperphagia). Conversely, electrical stimulation of this area results in the cessation of eating (hypophagia). Destructive lesions in the lateral hypothalamic area lead to hypophagia, even in the face of starvation,- electrical stimulation of this area initiates feeding activity, even when the animal has already eaten.
The regulation of eating behavior is part of a complex pathway that regulates food intake, energy expenditure, and reproductive function in the face of changes in nutritional state. In general, the hypothalamus regulates caloric intake, utilization, and storage in a manner that tends to maintain the body weight in adulthood. The presumptive set point around which it attempts to stabilize body weight, however, is poorly defined or maintained, as it changes readily with changes in physical activity, composition of the diet, emotional states, stress, pregnancy, and so on.
A key player in the regulation of body weight is the hormone leptin, which is released by white fat cells (adipocytes). As fat stores increase, plasma leptin levels increase, conversely, as fat stores are depleted, leptin levels decrease. Cells in the arcuate nucleus of the hypothalamus appear to be the sensors for leptin levels. Physiological responses to low leptin levels (starvation) are initiated by the hypothalamus to increase food intake, decrease energy expenditure, decrease reproductive function, decrease body temperature, and increase parasympathetic activity. Physiological responses to high leptin levels (obesity) are initiated by the hypothalamus to decrease food intake, increase energy expenditure, and increase sympathetic activity. Hypothalamic pathways involving neuropeptide Y are important for the starvation response, while pathways involving the melanocyte-stimulating hormone are important for the obesity response.
Review of Medical Physiology. 16th Ed. Norwalk, CT: Appleton & Lange, 1993.)
In addition to long-term regulation of body weight, the hypothalamus also regulates eating behavior more acutely. Factors that limit the amount of food ingested during a single feeding episode originate in the gastrointestinal tract and influence the hypothalamic regulatory centers. These include sensory signals carried by the vagus nerve that signify stomach filling and chemical signals giving rise to the sensation of satiety, including absorbed nutrients (glucose, certain amino acids, and fatty acids) and gastrointestinal hormones, especially cholecystokinin.
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