For 40 years, scientists searched for a mechanism by which the brain could monitor body fat deposition in order to keep an animal's body weight constant. In 1994, a gene that controlled the expression of a protein produced by adipose tissue was identified. Circulating levels of this protein (the ob protein) could be measured in normal weight mice. However, in obese ob/ob mice, which display marked overeating, this protein was absent due to a mutation of the ob gene. A series of studies demonstrated that the absence of this protein was responsible for over-consumption and obesity in the obese ob/ob. As the ob protein reduces food intake and also increases metabolic energy expenditure, both of which would result in weight loss, it was named leptin from the Greek 'leptos' meaning thin. In general, circulating levels of leptin appear to reflect the current status of body fat deposition and increase with the level of adiposity demonstrating the responsiveness of endogenous leptin to weight gain and energy status.
Since the identification of leptin and its receptor researchers have isolated numerous CNS hypothala-mic neuropeptide systems, which mediate the hypo-phagic action of leptin. NPY, the melanocortins, corticotropin releasing factor (CRF), cocaine and amphetamine regulated transcript (CART), and the orexins may all be part of the circuit linking adipose tissue with central appetite regulatory mechanisms. Certainly the fact that leptin has multiple effects on complex hypothalamic appetite systems, consisting of wide ranging but integrated regulatory neuropeptides, would appear to support the view that leptin is a major factor in body weight regulation. There is evidence of synergy between leptin and the short-term meal-generated satiety factor CCK. Systemic administration of CCK enhances leptin-induced decreases in food intake and augments weight loss in rodents.
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