Abstract 4370031: Targeting Asprosin For Treatment of Hypertension

Background: Hypertension is a leading risk factor for cardiovascular disease and is strongly associated with metabolic syndrome (MS), particularly obesity, through complex and multifactorial mechanisms. Asprosin, a recently discovered adipokine, has been positively correlated with several metabolic conditions, including obesity, type 2 diabetes, polycystic ovary syndrome (PCOS), fatty liver disease, and cardiovascular diseases such as coronary artery disease and hypertension. Asprosin’s two well-characterized metabolic roles include promoting hepatic gluconeogenesis and stimulating appetite by activating AgRP+ neurons in the hypothalamus. Furthermore, new findings suggest that asprosin signaling in the paraventricular nucleus causes a significant increase in blood pressure. In previous experiments, we demonstrated that neutralizing asprosin with anti-asprosin monoclonal antibodies significantly reduced appetite and corrected hyperglycemia in obese and diabetic mice. However, it remains unknown whether neutralizing asprosin also confers protection against hypertension. Hypothesis: We hypothesized that neutralization of asprosin signaling could serve as a viable therapeutic strategy for treating hypertension. Methods: We treated LepR db/db mice (a model of hypertension, type 2 diabetes, and obesity) and littermate controls (LepR db/+ ) with anti-asprosin monoclonal antibodies and measured blood pressure using the tail-cuff method. Results and Conclusion: Neutralizing asprosin significantly reduced the blood pressure of hypertensive LepR db/db mice. These findings suggest that targeting asprosin therapeutically may offer a promising "one remedy for three maladies" approach to simultaneously treat obesity, type 2 diabetes, and hypertension.