Increased asprosin in epididymal adipose tissue as a potential contributor to impaired vascular function in obese mice.

Vascular complications, such as impaired vasodilation, are a major problem that obese individuals face. In obesity, epididymal white adipose tissue (eWAT) expands, undergoes phenotypic changes, and begins to secrete a variety of adipokines that can metabolically regulate other organs and tissues including the cardiovascular system. Human studies report high levels of asprosin, a newly discovered adipokine secreted by WAT, in obesity. In this study, we hypothesize that obesity increases asprosin expression in eWAT which correlates to vascular complications.Eight-week-old male C57BL/6 mice were randomized into two experimental groups. The control group (n=7) received a standard chow diet (5% fat, 48.7% carbohydrates [3.2% sucrose]) and the Western Diet (WD) group (n=11) received a WD (40% fat, 43% carbohydrates [34% sucrose]) for 39 weeks. Obesity was confirmed by increased body weight (45.39 ± 1.98 g vs. 29.21 ± 0.79 g controls, p< 0.05) and increased BMI (0.45 ± 0.12 kg/m2 vs. 0.32 ± 0.01 kg/m2 controls, p< 0.05). At terminal experiments, eWAT was collected for histological and biochemical analysis. As expected, obese mice exhibited a greater amount of eWAT in comparison to the control group (2.69 ± 0.14 mg/g vs. 0.58 ± 0.06 mg/g controls, p< 0.05). Histological analysis of eWAT stained with H&E revealed that obesity induced a significant increase in adipocyte's size (10543.47 ± 694.06 μm2 vs.1726.64 ± 152.20 μm2 controls, p< 0.05) and infiltration of inflammatory cells surrounding adipocytes. Strikingly, greater asprosin expression was detected in eWAT from WD group in comparison to the control group (1.3 fold of increase, p<0.005). To assess whether asprosin has vascular effects, mesenteric arteries from control C57BL/6 mice were acutely incubated with pharmacological concentration of asprosin followed by vascular studies assessed by wire myograph. Our preliminary results show that asprosin impairs endothelium-dependent vasodilation (Emax:72.95% ± 7.38 vs. 93.33% ± 1.33 controls, n=3).The novelty of our results show that asprosin has a negative effect in vascular function. Our findings imply that eWAT may be a tissue contributing to the high levels of asprosin in obese individuals, further suggesting asprosin as a culprit of obesity-associated vascular dysfunction in obese males. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.