Abstract
Obesity has become a global health issue, but effective therapies remain very limited. Adaptive thermogenesis promotes weight loss by dissipating energy in the form of heat, thereby representing a promising target to counteract obesity. Notably, the regulation of thermogenesis is tightly orchestrated by complex neuronal networks, especially those in the hypothalamus. Recent evidence highlights the importance of adenosine monophosphate-activated protein kinase (AMPK) within the ventromedial nucleus of the hypothalamus (VMH) in modulating thermogenesis. Various molecules, such as GLP-1, leptin, estradiol, and thyroid hormones, have been reported to act on the VMH to inhibit AMPK, which subsequently increases thermogenesis through the activation of the sympathetic nervous system (SNS). In this review, we summarize the critical role of AMPK within the VMH in the control of energy balance, focusing on its contribution to thermogenesis and the associated mechanisms.
Highlights
Obesity and its related metabolic disorders, including type 2 diabetes, cardiovascular diseases and cancer, are major health threats which cause thousands of deaths per year in the contemporary society [1]
endoplasmic reticulum (ER) stress in the ventromedial nucleus of the hypothalamus (VMH) mediates the effects of AMPK on thermogenesis [52], suggesting that ER stress is another useful target for obesity
Designing drugs that act on the VMH to inhibit AMPK or ER stress might represent a promising approach for fighting against obesity
Summary
Obesity and its related metabolic disorders, including type 2 diabetes, cardiovascular diseases and cancer, are major health threats which cause thousands of deaths per year in the contemporary society [1]. Peripheral signals, such as thyroid hormones (THs), glucagon-like peptide-1 (GLP-1), estradiol (E2), bone morphogenetic proteins (BMP8B), and leptin, act on the VMH to promote BAT thermogenesis and WAT browning [16, 17]. Many hormones, such as THs, GLP-1, E2, BMP8B, and leptin, amplify the sympathetic tone to BAT and WAT by inhibiting AMPK activity in the VMH, resulting in enhanced thermogenesis and energy dissipation independent on food intake [16, 52, 64,65,66].
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