ABSTRACT
The prevalence of obesity in adults and children in the US and some European countries is growing at an alarming rate.[1] Several components of the mechanism that regulate energy homeostasis (the balance between food intake, storage and energy expenditure) have been identified.[2] One of the key elements is the satiety hormone, leptin.[3] Leptin, a 16 kDa hormone, is secreted from the adipocytes into circulation in proportion to body fat mass and reports to the brain on the status of energy reserves.[4] Even though the leptin receptor (lepR) is broadly expressed it was shown that its selective deletion in neurons, not in peripheral tissue, leads to obesity.[5] The activation of lepR, localized in the brain mainly in the hypothalamus, is believed to initiate a cascade of receptor-proximal and -distal neuropeptide-transmitted events that lead to the upregulation of anorexigenic (appetite suppressing) peptides and to the downregulation of orexigenic (appetite stimulating) ones.[6] In addition to its effects on food intake and body weight, leptin is known to regulate reproduction, carbohydrate metabolism, and bone formation.[7]
