Aging is associated with reduced vasodilation to insulin in subcutaneous adipose arteries in B6D2F1 mice

Abstract

The subcutaneous adipose tissue (sqAT) phenotype differs from that of the often studied visceral adipose tissue. Compared to visceral adipose, sqAT receives relatively less blood flow associated with lower rates of lipid mobilization and the promotion of long term lipid storage. Previously, we demonstrated endothelial dysfunction in arteries from visceral adipose of aged animals to be associated with impaired function in this adipose depot per se as well as with systemic metabolic dysfunction. Although the effect of aging on sqAT adipose arterial function is unknown, endothelial dysfunction in this depot may contribute to impaired lipid storage. The volume of the subcutaneous adipose per gram body mass, assessed by computed tomography, was reduced by 71% (P < 0.05) in old (28 – 31 mo; N = 5) compared to young (4 – 6 mo; N = 7) B6D2F1 mice. Contrary to our previous observation in visceral adipose arteries, dilation to acetylcholine was preserved with aging (92 ± 2 v 88 ± 4%, P > 0.05) and the nitric oxide inhibitor, LNAME, reduced dilation by ~38% in both groups (P < 0.05), indicating preserved nitric oxide dependent dilation in these arteries. However, dilation to insulin was lower in old mice (67 ± 2 v 42 ± 10%, P < 0.05) compared to young and LNAME did not abolish this difference, indicating a nitric oxide independent mechanism of dilatory dysfunction. Dilation in response to sodium nitroprusside was similar between groups (P > 0.05) indicating intact smooth muscle function. These data suggest that aging impairs insulin‐induced dilation in sqAT arteries, an effect that may have implications for altered lipid handling in advancing age.