scholarly journals Vitamin D Improves Nitric Oxide-Dependent Vasodilation in Adipose Tissue Arterioles from Bariatric Surgery Patients

Nutrients ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 2521 ◽  
Author(s):  
Abeer M. Mahmoud ◽  
Mary Szczurek ◽  
Chandra Hassan ◽  
Mario Masrur ◽  
Antonio Gangemi ◽  
...  

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.

Nutrients ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 2014 ◽  
Author(s):  
Mohamed Haloul ◽  
Smita Jagdish Vinjamuri ◽  
Dina Naquiallah ◽  
Mohammed Imaduddin Mirza ◽  
Maryam Qureshi ◽  
...  

There is a high prevalence of hyperhomocysteinemia that has been linked to high cardiovascular risk in obese individuals and could be attributed to poor nutritional status of folate and vitamin B12. We sought to examine the association between blood homocysteine (Hcy) folate, and vitamin B12 levels and vascular dysfunction in morbidly obese adults using novel ex vivo flow-induced dilation (FID) measurements of isolated adipose tissue arterioles. Brachial artery flow-mediated dilation (FMD) was also measured. Subcutaneous and visceral adipose tissue biopsies were obtained from morbidly obese individuals and non-obese controls. Resistance arterioles were isolated in which FID, acetylcholine-induced dilation (AChID), and nitric oxide (NO) production were measured in the absence or presence of the NO synthase inhibitor, L-NAME, Hcy, or the superoxide dismutase mimetic, TEMPOL. Our results demonstrated that plasma Hcy concentrations were significantly higher, while folate, vitamin B12, and NO were significantly lower in obese subjects compared to controls. Hcy concentrations correlated positively with BMI, fat %, and insulin levels but not with folate or vitamin B12. Brachial and arteriolar vasodilation were lower in obese subjects, positively correlated with folate and vitamin B12, and inversely correlated with Hcy. Arteriolar NO measurements and sensitivity to L-NAME were lower in obese subjects compared to controls. Finally, Hcy incubation reduced arteriolar FID and NO sensitivity, an effect that was abolished by TEMPOL. In conclusion, these data suggest that high concentrations of plasma Hcy and low concentrations of folate and vitamin B12 could be independent predictors of vascular dysfunction in morbidly obese individuals.


2018 ◽  
Vol 14 (11) ◽  
pp. S136-S138
Author(s):  
David Romero Funes ◽  
David Gutierrez Blanco ◽  
Maria C Fonseca Mora ◽  
Rama Rao Ganga ◽  
Emanuele Lo Menzo ◽  
...  

2020 ◽  
Vol 20 (8) ◽  
pp. 1282-1294
Author(s):  
Meroua Bouchemal ◽  
Djennat Hakem ◽  
Malha Azzouz ◽  
Chafia Touil-Boukoffa ◽  
Dalila Mezioug

Background: Metabolic syndrome (MetS) is a combination of metabolic disorders with increased risks for several diseases, such as cardiovascular diseases and diabetes. It is associated with the presence of various inflammatory molecules. Vitamin D plays an important role in the regulation of metabolism homeostasis. Objective: The main goal of this work is to investigate vitamin D levels among Algerian MetS patients and its possible outcomes on key molecules of the immune response, as well, the immunomodulatory effects of its active metabolite. Methods: We evaluated vitamin D status by the electrochemiluminescence method, Nitric Oxide (NO) levels by the Griess method and Matrix Metalloproteinases (MMPs) activities such as MMP-2 and MMP-9 by zymography in plasma of patients and healthy controls (HC). The immunomodulatory effects of the active metabolite of vitamin D (α-25 (OH)2D3) on the production of NO, IL-6, IL-10, TGF- β and s-CTLA-4 were assessed by Griess method and ELISA, in peripheral blood mononuclear cells (PBMCs) of Algerian MetS patients and HC. MMPs activities were also determined ex-vivo, while iNOS expression was assessed by immunofluorescence staining. Results: Severe vitamin D deficiency was registered in Algerian MetS patients. The deficiency was found to be associated with an elevated in vivo NO production and high MMPs activity. Interestingly, α-25 (OH)2D3 declined the NO/iNOS system and IL-6 production, as well as MMPs activities. However, the ex-vivo production of IL-10, TGF-β increased in response to the treatment. We observed in the same way, the implication of s-CTLA-4 in MetS, which was markedly up-regulated with α-25 (OH)2D3. Conclusion: Our report indicated the relationship between MetS factors and Vitamin D deficiency. The ex-vivo findings emphasize its impact on maintaining regulated immune balance.


2012 ◽  
Vol 108 (11) ◽  
pp. 1915-1923 ◽  
Author(s):  
Cherlyn Ding ◽  
Dan Gao ◽  
John Wilding ◽  
Paul Trayhurn ◽  
Chen Bing

Vitamin D deficiency and the rapid increase in the prevalence of obesity are both considered important public health issues. The classical role of vitamin D is in Ca homoeostasis and bone metabolism. Growing evidence suggests that the vitamin D system has a range of physiological functions, with vitamin D deficiency contributing to the pathogenesis of several major diseases, including obesity and the metabolic syndrome. Clinical studies have shown that obese individuals tend to have a low vitamin D status, which may link to the dysregulation of white adipose tissue. Recent studies suggest that adipose tissue may be a direct target of vitamin D. The expression of both the vitamin D receptor and 25-hydroxyvitamin D 1α-hydroxylase (CYP27B1) genes has been shown in murine and human adipocytes. There is evidence that vitamin D affects body fat mass by inhibiting adipogenic transcription factors and lipid accumulation during adipocyte differentiation. Some recent studies demonstrate that vitamin D metabolites also influence adipokine production and the inflammatory response in adipose tissue. Therefore, vitamin D deficiency may compromise the normal metabolic functioning of adipose tissue. Given the importance of the tissue in energy balance, lipid metabolism and inflammation in obesity, understanding the mechanisms of vitamin D action in adipocytes may have a significant impact on the maintenance of metabolic health. In the present review, we focus on the signalling role of vitamin D in adipocytes, particularly the potential mechanisms through which vitamin D may influence adipose tissue development and function.


2020 ◽  
Vol 45 (10) ◽  
pp. 1092-1098
Author(s):  
Soodabeh Aliashrafi ◽  
Mehrangiz Ebrahimi-Mameghani ◽  
Mohammad Asghari Jafarabadi ◽  
Lida Lotfi-Dizaji ◽  
Elnaz Vaghef-Mehrabany ◽  
...  

As there is limited and inconsistent evidence in potential role of vitamin D on insulin resistance and matrix metalloproteinases, this study aimed to examine the effect of vitamin D supplementation on glucose homeostasis, insulin resistance, and matrix metalloproteinases in obese subjects with vitamin D deficiency. A total of 44 participants with serum 25-hydroxyvitamin D (25(OH)D) level ≤ 50 nmol/L and body mass index (BMI) 30–40 kg/m2 were randomly allocated into receiving weight reduction diet with either 50 000 IU vitamin D3 pearl (n = 22) or placebo (n = 22) once weekly for 12 weeks. Primary outcomes were changes in fasting serum glucose (FSG), homeostasis model assessment of insulin resistance (HOMA-IR), quantitative insulin sensitivity check index (QUICKI), and matrix metalloproteinases (MMPs). Secondary outcomes were changes in weight, BMI, 25(OH)D, calcium, phosphorous and parathyroid hormone (PTH). Sun exposure and dietary intakes were also assessed. Serum levels of 25(OH)D3 increased significantly with a simultaneous decrease in serum concentration of PTH in the vitamin D group. Weight, BMI, FSG, and MMP-9 decreased significantly in both groups, and there were significant differences in changes in weight, serum 25(OH)D3, PTH, and MMP-9 levels between the groups. Within- and between-groups analysis revealed no significant differences in serum calcium, phosphorous, serum insulin, HOMA-IR, QUICKI, and MMP-2 after intervention. Our results indicated that improvement in vitamin D status resulted in greater reductions in weight and MMP-9 during weight loss. These preliminary results are sufficient to warrant a bigger study group.


2012 ◽  
Vol 93 (1) ◽  
pp. 82-90 ◽  
Author(s):  
Gaurav K. Gupta ◽  
Tanupriya Agrawal ◽  
Michael G. DelCore ◽  
Syed M. Mohiuddin ◽  
Devendra K. Agrawal

2012 ◽  
Vol 97 (7) ◽  
pp. E1229-E1233 ◽  
Author(s):  
G. H. E. J. Vijgen ◽  
N. D. Bouvy ◽  
G. J. J. Teule ◽  
B. Brans ◽  
J. Hoeks ◽  
...  

2016 ◽  
Vol 34 (4_suppl) ◽  
pp. 165-165 ◽  
Author(s):  
Kiran Virik ◽  
Robert Wilson

165 Background: Metabolic bone disease is a known but incompletely understood consequence of gastrectomy. Post gastrectomy osteoporosis (OP) is multifactorial. Evidence suggests that patients who undergo this surgery require long term bone health assessment and nutritional support. Methods: 30 post gastrectomy patients (2000-2008) from a single centre in Australia were evaluated re bone health post surgery and post nutritional supplementation. Exploratory analysis included: age, gender, pathology, type of surgery, 25 OH-vitamin D, calcium, parathyroid hormone (PTH), bone mineral density (BMD), vertebral XRs, urinary calcium and N telopeptides of type I collagen. Other risk factors evaluated were: smoking, corticosteroid use, alcohol intake, hyperthyroidism, menopausal status, hyperparathyroidism (hPTH), pre-existing bone disease. Results: The median age of the cohort was 67.5 (range 53-83) of whom 22 (73%) were male. Histology showed 16 (53%) gastric adenocarcinoma, 6 (20%) esophageal adenocarcinoma, 2 (7%) GISTs, 5 (17%) gastric/duodenal lymphoma and 1 other category. Similar numbers of patients underwent total (12) and partial/distal gastrectomy (12), with 6 having a subtotal gastrectomy. 22 (73%) had a Roux-en-Y or BR II reconstruction and 8 had a BRI/other. Median time from surgery to first BMD was 54.5 months (range 12-360) with median correlative calcium level 2.24 (range 1.97-2.49), median vitamin D level 43 (range 11-82) and median PTH 6.4 (range 1.8-13.8). Osteoporosis was diagnosed in 14 (47%) of patients, osteopenia in 14 and 2 (7%) patients had a normal BMD. Low vitamin D was seen in 23 (77%) patients, low calcium levels in 5 (17%) and secondary hPTH in 12 (41%). Post nutritional supplementation preliminary results showed 2/23 (9%) had a low vitamin D level, 3/11 (27%) had secondary hPTH, 5/19 (26%) had osteoporosis, 12/19 (63%) had osteopenia and 2/19 had a normal BMD. Analysis of other risk factors is to follow. Conclusions: Poor bone health and vitamin D deficiency is a clinically significant problem post gastrectomy. Patients should undergo long term nutritional and bone health surveillance in addition to their oncological follow up post resection.


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