Asprosin (ASP) is a newly discovered glucogenic protein hormone in 2016, it is mainly produced and secreted by adipocytes and can act on a variety of tissues and organs. Current studies have found that ASP targets the liver by binding to the Olfr734 receptor, promoting hepatic glucose release and maintaining blood sugar balance; affects the activity of feeding neurons and increases appetite after crossing the blood-brain barrier; acts on fat, inhibits the browning of white fat and promotes adipogenesis; acts on the pancreas, inhibits β-cell autophagy and promotes β-cell inflammation; acts on skeletal muscle, reduces insulin sensitivity. Therefore, ASP is involved in regulating the occurrence and development of diseases such as obesity, diabetes, insulin resistance and polycystic ovarian syndrome, and is expected to become a new molecular target for the treatment of metabolic diseases. The changes of ASP levels in pathological states may be quite different in people of different ages, genders and obesity levels. It is not clear whether the elevated ASP levels are a consequence of disease or a protective feedback mechanism under disease states. The research on ASP and metabolic syndrome mostly focuses on the causal relationship, and more molecular mechanisms are needed to reveal the function and role of ASP. ASP stimulates the release of sex hormones through the hypothalamus-pituitary-gonadal axis, improves sperm parameters, and affects reproductive function. The increase in ASP in pathological conditions inhibits reproductive potential, but this decline in reproductive potential needs to be further confirmed by knocking out the FBN gene, the knockout of Olfr734 receptor cannot fully explain the effect of ASP gene on reproduction. In addition, whether the effect of ASP on testosterone is only centrally and not peripherally, further studies are needed to confirm. Revealing the effect of ASP gene on reproductive function will help to explain the molecular mechanism of adipokines involved in regulating male reproductive function. Exercise is an effective means to improve metabolic syndrome and enhance reproductive function. Exercise can regulate the level of adipokines. At present, there are few studies on exercise and ASP, and there is controversy. Only by increasing the experimental research on the effect of exercise on ASP can better explain the exact effect of exercise on ASP; exercise can also reverse the reproductive effect caused by metabolic imbalance. Functional decline, the relationship between exercise and ASP and reproduction in metabolic syndrome can be explored in the future.