Elevated asprosin in postmenopause is associated with vasculometabolic complications.

Abstract

Postmenopause is associated with increased adiposity, metabolic syndrome, and heightened cardiovascular disease (CVD) risk, yet the adipose-derived factors potentially contributing to vascular impairment remain poorly defined. Asprosin, a glucogenic adipokine secreted by white adipose tissue (WAT), is elevated in metabolic diseases; however, its association with postmenopausal vascular complications remains unknown. In this study, we investigated circulating and adipose tissue asprosin levels in a long-term ovariectomy (OVX) mouse model of postmenopause. Female mice underwent OVX or sham surgery and were followed for 20 wk. OVX mice developed typical postmenopausal bone porosity, specifically in the lumbar vertebrae, along with cardiometabolic disorders, including weight gain, increased adiposity, metabolic syndrome-like alterations, and significant arterial stiffness, an early vascular insult marker. Notably, these postmenopausal changes were associated with elevated circulating asprosin levels and increased asprosin expression in subcutaneous adipose tissue. Results from ex vivo wire myography studies demonstrated that asprosin directly potentiates vasoconstriction, implying that asprosin exerts a direct vascular effect. Together, these findings provide novel evidence of an association between elevated asprosin and postmenopausal vasculometabolic alterations. These observations support further investigation of asprosin as a potential biomarker of cardiometabolic and vascular changes and as a candidate for future investigation.Postmenopause is a critical period in women's lives marked by metabolic and vascular changes that remain poorly understood. Asprosin, a novel adipokine, is linked to metabolic disorders and cardiovascular risk. In long-term OVX mice, circulating asprosin levels were elevated and associated with weight gain and arterial stiffness. Exogenous asprosin was associated with vasoconstriction, supporting its potential as a biomarker and a candidate for further mechanistic investigation in postmenopausal vasculometabolic regulation.