Today, excessive nutrition and sedentary life have brought along many chron-ic diseases such as obesity and diabetes. As is known, obesity is a disorder of both energy metabolism and appetite regulation. In re-cent studies, it has been reported that AMPK regu-lates the metabolic energy balance as well as governs appetite control. When AMPK is activated, anabol-ic reactions are inhibited, while catabolic reactions are activated to produce energy. In addition to many pharmacological drugs and nutritional supplements, exercise activates AMPK and enhances the translo-cation of the glucose trans-porter (GLUT4) protein, which provides insulin-independent cellular glu-cose uptake. AMPK is an essential intracellular sensor against obesity because when AMP and LKB1 acti-vate AMPK, the use of body fat stores will be en-couraged to produce energy. Appetite-stimulating and suppressing agents act on AMPK to regulate both food intake and body weight control. When appe-tite suppressors such as leptin, insulin, metformin, inhibit AMPK leucine, and berberine, the expression of orexigenic neuropeptides are decreased while the expression of anorexigenic neuropeptides is increased. Understanding the mecha-nisms controlled by the hypothalamic AMPK is crucial for developing ef-fective nutritional strategies for the treatment of nutri-tional intake disorders such as obesity, diabetes mellitus, cardiovascular disease, hypertension and cancer.
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