Abstract

High-fat Diet (HFD) induced obesity is known as a model of mostly closed to human obesity condition. DIO not only induces peripheral insulin resistance, and glucose intolerance but also impairs central leptin and insulin signaling pathways. Exercise training reduces adiposity by mainly increased energy expenditure, however, the underlying mechanism associated with central nervous system remains largely unknown. This article highlights the recent publication by Laing et al, who first demonstrated that voluntary exercise enhanced POMC-expressing neuron survival rate in the hypothalamus of mice by protecting from apoptosis induced by long-term HFD induced obesity, improved central leptin sensitivity, and systemic insulin sensitivity, shed a light on the central mechanism of exercise improves metabolic function.

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