Why the study?
Pathophysiological mechanisms linking vitamin-D deficiency in obesity to unfavorable cardiometabolic outcomes remain unestablished.
Does ex vivo 1,25-dihydroxyvitamin D improve nitric oxide-dependent vasodilation in adipose tissue arterioles from morbidly obese adults?
Does ex vivo 1,25-dihydroxyvitamin D improve nitric oxide-dependent vasodilation in adipose tissue arterioles from morbidly obese adults?
Vitamin D improves nitric oxide-dependent arteriolar vasodilation in adipose tissue from obese adults, suggesting a potential mechanism for mitigating obesity-related microvascular dysfunction.
Answers are grounded in this paper and cite their sources.
May support vitamin D in obesity-related microvascular dysfunction; hypothesis-generating and requires clinical trials before practice change.
There is a high prevalence of vitamin-D deficiency in obese individuals that could be attributed to vitamin-D sequestration in the adipose tissue. Associations between vitamin-D deficiency and unfavorable cardiometabolic outcomes were reported. However, the pathophysiological mechanisms behind these associations are yet to be established. In our previous studies, we demonstrated microvascular dysfunction in obese adults that was associated with reduced nitric oxide (NO) production. Herein, we examined the role of vitamin D in mitigating microvascular function in morbidly obese adults before and after weight loss surgery. We obtained subcutaneous (SAT) and visceral adipose tissue (VAT) biopsies from bariatric patients at the time of surgery (n = 15) and gluteal SAT samples three months post-surgery (n = 8). Flow-induced dilation (FID) and acetylcholine-induced dilation (AChID) and NO production were measured in the AT-isolated arterioles ± NO synthase inhibitor N(ω)-nitro-L-arginine methyl ester (L-NAME), hydrogen peroxide (H2O2) inhibitor, polyethylene glycol-modified catalase (PEG-CAT), or 1,25-dihydroxyvitamin D. Vitamin D improved FID, AChID, and NO production in AT-isolated arterioles at time of surgery; these effects were abolished by L-NAME but not by PEG-CAT. Vitamin-D-mediated improvements were of a higher magnitude in VAT compared to SAT arterioles. After surgery, significant improvements in FID, AChID, NO production, and NO sensitivity were observed. Vitamin-D-induced changes were of a lower magnitude compared to those from the time of surgery. In conclusion, vitamin D improved NO-dependent arteriolar vasodilation in obese adults; this effect was more significant before surgery-induced weight loss.
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Mahmoud et al. (2019) studied this question.
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