Abstract
Leptin, which is a product of the obese gene (ob), was first identified in 1994. Mutations in the leptin gene or its receptor result in obesity in rodents by increasing the desire for food intake, reducing energy expenditure, and increasing insulin secretion. These mutations also result in many other neuroendocrine and metabolic abnormalities. Leptin has been shown to inhibit neuropeptide Y neurons in the arcuate nucleus of the hypothalamus. These neurons are believed to cause energy gain in order to defend body weight and restore energy balance. The increase in neuropeptide Y could also explain the decrease in gonadotropin secretion, poor reproductive function, decreased thyroid activity, and other endocrine abnormalities. However, it is likely that there are other points of impact of leptin in the control of appetite, as shown by the reduced feeding in the neuropeptide Y knockout mouse.
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