Leptin human brain

Leptin is a cytokine produced and secreted by adipose tissue in proportion to the body fat content [3]. Mice and humans lacking leptin or its receptor develop a severe hyperphagia and a dramatic degree of obesity which is considerably more pronounced than that of the NDRKO mouse. Thus, leptin is the key adiposity signal in rodents and humans. Leptin secretion appears to reflect the metabolic status of the adipocyte rather than the sheer size of triglyceride deposits, and leptin levels may transiently be dissociated from total body fat. Nonetheless, over the course of a day with unrestricted food supply, plasma leptin levels reliably reflect the amount of total body fat. Local administration of leptin into the brain results in reduced food intake. The vast majority of patients with obesity have elevated serum levels of leptin. Thus, it is believed that the polygenic obesity is due to leptin resistance rather than to inadequate leptin secretion, or to a reduced blood/brain transport of the cytokine. 

The regulation of food intake in humans is complex. In addition to genetic and cultural influences, it involves the action of leptin, insulin, ghrelin, PYY, cholecystokinin, and amylin. Most of these molecules act by signaling to the brain. 

Subsequent work revealed that the "satiety factor" is a protein called Jeptinand that its target is a receptor in the hypothalamus. Attention to the cause of human obesity has focused on changes in the structure of the Jeptin receptor, defects in the mechanism of transport of serum leptin to the brain (Schwartz ef aL, 1996 Caro et al., 1996), and on mutations that affect the signaling proteins that respond to the leptin receptor... 

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