Glucose stimulated adipose tissue blood flow is reduced after high fat feeding despite diminished resistance artery vasoconstrictor reactivity (1072.9)

Fasted adipose tissue blood flow (ATBF) supplies energy via transport of stored free fatty acids, whereas after feeding ATBF increases to reduce circulating free fatty acids. Although high fat diet (HF; 40% Kcal fat) has been demonstrated to reduce endothelium dependent dilation in epididymal white adipose tissue (eWAT) resistance arteries, the effect of HF on eWAT artery vasoconstrictor reactivity is unknown. Here, we examined basal and glucose stimulated (2 g/kg, ip, 15 min) ATBF using radiolabelled microspheres as well as vasoconstrictor responses in eWAT resistance arteries in young normal chow (NC: 14% Kcal fat) and HF fed male B6D2F1 mice. Basal ATBF (eWAT) was not different in HF (0.20 ± 0.1 v 0.08 ± 0.02 %Cardiac Output, p > 0.05) compared to NC mice. Glucose stimulation increased ATBF 5‐fold in NC (p = 0.03) but this increase was blunted in HF mice (1.6‐fold, P=0.09). Although KCl‐induced eWAT vasoconstriction did not differ between diet groups, HF blunted maximal vasoconstriction to norepinephrine (26%), angiotensin‐II (35%), and endothelin‐1 (11%) compared with NC (All p < 0.05). In the face of diminished endothelium dependent dilation and reduced nitric oxide, reductions in vasoconstrictor reactivity may preserve basal ATBF in HF mice. However, enhanced vasoconstriction does not play a role in the diminished hyperemic response to glucose in adipose tissue after HF.