Multiple studies tend to link various forms of obesity in humans with genetic mutations. The most serious track is that of leptin. The ob gene, which codes for this protein, is expressed only in white adipose tissue. Leptin would be secreted by this tissue and would slow down eating behavior by a hypothalamic relay. Its absence would be responsible for the metabolic abnormalities observed in mutant mice for this gene (obesity, hyperinsulinemia, hyperglycemia, hypothermia). In rats, the production of leptin by adipose tissue collapses within a few hours of fasting or during experimental diabetes and returns to normal in a few hours too, after resumption of feeding or administration of insulin. This type of hormonal regulation as strict as this clearly indicates that leptin would act as a signal of satiety.
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In addition, the administration of leptin to genetically obese mice results in very impressive weight loss. Leptin also works on healthy animals which can lose 12%. 100 of their body weight and all their fat in four days. Finally, intracerebral administration is more effective than intraperitoneal administration, an observation which supports a central receptor site.
But what about in humans? The results obtained are surprising: the product of the ob gene is greatly increased in all obese people. This increase is proportional to the total body mass. It is more marked in female subjects, which indicates that leptin is subject to an additional level of hormonal regulation. In addition, no mutation is observed in the region where the mutation that makes the mouse obese resides. It is therefore clear that obesity is not due to a reduced synthesis of leptin nor to the production of an abnormal leptin.