ABSTRACT
The brainstem regulates meal size in response to satiety signals. Both humoral and neural satiety signals exist to inhibit feeding. According to the glucostatic hypothesis a transient fall in blood glucose is responsible for initiating feeding. The anxiety hypothesis starts from the premise that when anorexic women eat, they become anxious, and the well documented finding that anorexics show enhanced secretion of corticotrophin releasing hormone (CRH) and glucocorticoids. Feeding stimulates the secretion of cholecystokinin which apart from being a satiety factor also excites CRH secretion. The effect of leptin and centrally acting insulin on food intake is brought about by a decrease in the secretion of neuropeptide Y, which is both the most potent stimulator of feeding known, and the most abundant neuropeptide in the brain. In general, mice with obesity, whether genetic or acquired, have high plasma concentrations of leptin which reflects their adiposity.
