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The central nervous system (CNS) orchestrates the whole-body metabolism. Within the CNS, the hypothalamus plays a dominant role in the regulation of metabolic homeostasis in response to dynamic challenges such as hypoglycemia, cold-exposure, and exercise. Our previous work articulates that neurons in the dorsomedial and central parts of ventromedial hypothalamic nucleus (VMHdm/c neurons) substantially contribute to metabolic adaptations to exercise training including augmented skeletal muscle mass and basal metabolic rate in mice. Knockdown of steroidogenic factor-1 (SF-1) in VMHdm/c neurons hampers exercise-induced mRNA expression of peroxisome proliferator-activated receptor gamma coactivator 1 alpha (Pgc-1α) in skeletal muscle. PGC-1α is a key transcriptional regulator that controls a broad range of genes related to glucose and fat metabolism, mitochondrial functionangiogenesis, and protein synthesis. Loss- or gain-of-function of PGC-1α in skeletal muscle dramatically changes skeletal muscle physiology as well as whole-body metabolism. These data suggest that VMHdm/c neurons expressing SF-1 (VMHdm/cSF-1 neurons) mediate metabolic responses of skeletal muscle to exercise, thereby contributing to metabolic benefits of exercise. However, the mechanisms by which VMHdm/cSF-1 neurons mediate exercise-induced augmented skeletal muscle PGC-1α expression remains unclear. In particular, the pathway from VMHdm/cSF-1 neurons to skeletal muscle has yet to be unraveled.


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Pavlo Petakh, Iryna Kamyshna, Aleksandr Kamyshnyi

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2021 impact factor: 8.568

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