Microvascular vasodilator function is impaired in obese patients, with little further impairment in impaired fasting glucose and type 2 diabetes patients
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The relative roles of endothelium vs vascular smooth muscle impairment in vascular dysfunction in patients spanning the spectrum of obesity to impaired fasting glucose (IFG) and type 2 diabetes are not well established. To assess the impact of obesity and diabetes on vascular relaxation in human subjects, the forearm resistance vessel responses to intra-arterial vasoactive agents (endothelium-dependent, endothelium-independent, and adrenergic stimuli) were studied in matched subjects on no antihyperglycaemic medications classified in 4 groups: type 2 diabetes, impaired fasting glucose (IFG), obese, and nonobese. Compared to nonobese subjects, responses to both acetylcholine and nitroprusside were impaired in obese, IFG and diabetic subjects. Compared to normoglycaemic obese subjects, diabetic and IFG subjects demonstrated no further impairment. Gender-specific data revealed that compared to nonobese males, obese, IFG, and diabetic males showed impaired responses to nitroprusside whereas compared to nonobese females, obese, IFG, and diabetic females showed impaired responses to acetylcholine. Using multivariate analyses, gender and adiposity, but not glycaemia, were strongly related to acetylcholine and nitroprusside responses. By contrast, vasoconstriction to norepinephrine was greater in subjects with diabetes and IFG compared to nondiabetic obese controls. These results underscore the input of obesity and body fat in the pathogenesis of resistance vessel dysfunction.
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