Abstract
The discovery that the hormone leptin regulates adipose tissue mass through hypothalamic effects on both satiety and energy expenditure, has led to research to determine whether mutations of the leptin receptor lead to obesity in humans and laboratory animals. In rodents, homozygous mutations in genes that encode leptin or the leptin receptor have been reported to cause early onset morbid obesity, increased appetite, and decreased energy utilization. Interestingly, these laboratory rats also exhibit endocrine alterations, including hypercortisolemia and hypogonadotropic hypogonadism. There are also reports …
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