Abstract
Reproduction is an energy demanding function and only take place in case of sufficient available energy status in mammals. Metabolic diseases such as anorexia nervosa are clinically associated with reduced fertility. AMP-activated protein kinase (AMPK), as a major regulator of cellular energy homeostasis, is activated in limited energy reserves to ensure the orderly progress of various physiological activities. In recent years, mounting evidence shows that AMPK is involved in the regulation of reproductive function through multiple mechanisms. AMPK is likely to be a metabolic sensor integrating central and peripheral signals. In this review, we aim to explore the preclinical studies published in the last decade that investigate the role of AMP-activated protein kinase in the reproductive field, and its role as a target for drug therapy of reproductive system-related diseases. We also emphasized the emerging roles of AMPK in transcriptional regulation of reproduction processes and metabolisms, which are tightly related to the energy state and fertility of an organism.
Highlights
AMP-activated protein kinase (AMPK) is a heterotrimeric complex composed of a catalytic α-subunit and two regulatory subunits: β and γ
A large body of research has shown that AMPK is not limited to serve as a major energy sensor to monitor the supply of nutrients, and involved in the regulation of reproduction through several different strategies
AMPK affects the secretion of gonadotropin-releasing hormone (GnRH) and gonadotropins and integrates energy status with fertility at the level of the hypothalamus and pituitary
Summary
AMP-activated protein kinase (AMPK) is a heterotrimeric complex composed of a catalytic α-subunit and two regulatory subunits: β and γ. In response to decreased ATP/AMP ratio or glucose starvation, the liver kinase B1 (LKB1) phosphorylates the threonine-172 residue of AMPK and mediates its activation through canonical and non-canonical mechanisms. These two activation mechanisms occur in the cytoplasm and lysosome, respectively (Gonzalez et al, 2020). AMPK switches off ATP-consuming pathways such as protein synthesis, glycogenolysis, and lipogenesis, and turns on ATP-generating pathways such as fatty acid oxidation, glycolysis, and autophagy by regulating downstream factors, thereby ensuring nutrient supply (Hardie, 2007)
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