Leptin signaling correction is the clinical and biological process of restoring the normal sensitivity and responsiveness of central and peripheral tissues to the satiety hormone, leptin. Leptin resistance, characterized by high circulating leptin levels without the expected metabolic effects, is a common feature of obesity and metabolic dysfunction. Achieving correction is essential for normalizing appetite regulation, energy expenditure, and overall body weight set point.
Origin
This concept arose following the discovery of leptin, a hormone secreted by adipocytes, and the subsequent realization that many obese individuals exhibited hyperleptinemia and a failure to respond to its signals. The term reflects the therapeutic goal of overcoming this resistance, a key challenge in the field of neuroendocrinology and weight management. It focuses on the brain’s ability to accurately interpret the body’s energy status.
Mechanism
Correction involves mitigating the factors that interfere with leptin’s transport across the blood-brain barrier and its binding to the long-form leptin receptor (LepRb) in the hypothalamus. Chronic inflammation and excessive free fatty acids can impair this signaling cascade, particularly the JAK-STAT pathway, which transmits the satiety signal. Restoring sensitivity allows leptin to effectively suppress appetite and promote thermogenesis, thereby re-establishing energy balance.
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