The Interaction of Obesity and Ghrelin/Leptin

The incidence of obesity, the most important health problem in the developing world, has increased dramatically both adults and children in recent years. Obesity usually occurs with limited actions and unbalanced received/spent energy. Obesity is the basis for the formation of many metabolic diseases and a component of metabolic syndrome accompanied by hypertension, insulin resistance, high triglyceride and low HDL concentrations. The hypothalamus is the brain region in which hunger and satiety are managed by signals of the peripheral polypeptite hormones the release from peripheral organs. In mammals, the peripheral peptite identified as oreksigen and an appetite enhancer is the ghrelin hormone. Ghrelin is produced by the fundus region cells and released in the circulation. It binds to growth hormone stimulating receptors and induces food intake through the arcuate nucleus neuropeptite Y (NPY) and arguate-associated peptite (AgRP) in the hypothalamus. Leptin, which is antagonist to ghrelin and expressed by adipose tissue, inhibits AgRP and NPY activity while activating pro-opiomelanocortin (POMC) and cocaine and amphetamine-regulated transcript (CART) in the hypothalamus and suppressing appetite. The quality of the food and the mutations in receptors or genes of these hormones are significantly caused for the pathogenesis of obesity. The aim of this review, in the light of current studies, is to focus on the obesity and relationship between ghrelin and leptin hormones stimulating of hunger / satiety signals in the hypothalamus and provide an approach to the use of agonists or antagonists of these hormones as a treatment option