Vitamin D limits inflammation-linked microRNA expression in adipocytes <i>in vitro</i> and <i>in vivo</i>: A new mechanism for the regulation of inflammation by vitamin D

Karkeni, Esma; Bonnet, L.; Marcotorchino, Julie; Tourniaire, Franck; Astier, Julien; Ye, Jianping; Landrier, Jean‐François

doi:10.1080/15592294.2016.1276681

Cited by 88 publications

(80 citation statements)

References 46 publications

(56 reference statements)

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“…Vitamin D is a micronutrient that was earlier known only for its role in bone mineral homeostasis. In recent years, it has gained the reputation of being a pleiotropic regulator of biological functions ranging from cell cycle regulation to inflammation . Among its extraskeletal effects, its role in cardiometabolic diseases remains a subject of interest.…”

Section: Discussionmentioning

confidence: 99%

“…In recent years, it has gained the reputation of being a pleiotropic regulator of biological functions ranging from cell cycle regulation to inflammation. [17,18] Among its extraskeletal effects, its role in cardiometabolic diseases remains a subject of interest. While a large number of studies have reported association between vitamin D deficiency and adverse cardiovascular as well as metabolic outcomes in patients, lack of adequate causal insights needs to be addressed.…”

Section: Discussionmentioning

confidence: 99%

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Vitamin D Deficiency in Rats Causes Cardiac Dysfunction by Inducing Myocardial Insulin Resistance

Nizami

Katare

Prabhakar

et al. 2019

Molecular Nutrition Food Res

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Scope Cause‐effect relationship between vitamin D deficiency and cardiometabolic abnormalities remains undefined. The aim is to investigate the role of vitamin D deficiency in cardiac failure, through possible involvement in myocardial insulin signaling. Methods and results Male SD rats (n = 6) are fed a normal diet (Con), vitamin D‐deficient diet [Con(‐)], or high‐fat, high fructose diet (HFHFrD) for 20 weeks. Cardiac hypertrophy and fetal gene program are confirmed in Con(‐) group. Cardiac dysfunction is assessed by echocardiography. Elevated renin, TGF‐β and collagen‐1α mRNAs, p‐ERK1/2, and perivascular fibrosis indicate cardiac remodeling in Con(‐) group. Increased serum insulin, triglycerides, and blood pressure, and decreased glucose tolerance and HDL cholesterol are observed in Con(‐) rats. Decreased p‐Akt/Akt, GLUT4, SOD2, and catalase, and increased NF‐κB, TNF‐α, and IL‐6 are observed in Con(‐) hearts. In H9c2 cells, calcitriol attenuates palmitate‐induced insulin resistance. VDR‐silenced H9c2 cells show reduced Akt phosphorylation, GLUT4 translocation, and 2‐NBDG uptake. Findings in Con(‐) and HFHFrD groups are comparable. Conclusion Vitamin D deficiency in rats mimic high‐fat‐, high‐fructose‐induced metabolic syndrome and cardiac dysfunction. This study demonstrates that vitamin D deficiency is an independent risk factor for heart failure, at least in part, through induction of myocardial insulin resistance.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Vitamin D Deficiency in Rats Causes Cardiac Dysfunction by Inducing Myocardial Insulin Resistance

Nizami

Katare

Prabhakar

et al. 2019

Molecular Nutrition Food Res

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“…The ability of vitD to deactivate NF-κB signaling, via p65 and IκB phosphorylation inhibition in murine adipocytes, was observed and could constitute a driving molecular mechanism (Fig. 1) [60].…”

Section: Vitd and Inflammationmentioning

confidence: 98%

“…VitD exerts anti-inflammatory effects mediated by the inhibition of the NF-κB and mitogen activated protein kinase signaling pathways [60]. Additionally, vitD reduced toll-like receptor expression, which is increased in both immune cells and AT from people with obesity [63][64][65].…”

Section: Vitd and Inflammationmentioning

confidence: 99%

Genetic Factors and Molecular Mechanisms of Vitamin D and Obesity Relationship

et al. 2018

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Vitamin D (vitD) deficiency is associated with a wide range of chronic diseases and conditions, including obesity, and with an increasing severity of metabolic dysregulation, such as insulin resistance, hyperlipidemia, liver disease, and hypertension, both in children and adults. However, the nature of the association between low vitD status and obesity remains unclear. This fact has motivated the scientific community to conduct genetic association analyses between 25-hydroxyvitamin D (25[OH]D)-related genes and obesity traits. In this line, the variation in the vitD receptor (VDR) gene represents the bulk of the findings. Specifically, polymorphisms in the VDR gene have been associated with obesity traits in some but not all, studies. Thus, results regarding this matter remain inconclusive. Other genes aside from VDR have also been investigated in relation to obesity-related traits. However, again, findings have been inconsistent. In general, results point to the fact that the DBP/GC gene could be an important protein-linking obesity and vitD status. On the other hand, several studies have attempted to determine the molecular mechanism of the relationship between 25(OH)-D levels and obesity. Some of these studies suggest that vitD, due to its fat-soluble characteristic, is retained by the adipose tissue and has the capacity to metabolize 25(OH)-D locally, and this can be altered during obesity. Additionally, vitD is capable of regulating the gene expression related to adipogenesis process, inflammation, oxidative stress, and metabolism in mature adipocytes. Therefore, the aim of the present review was to evaluate the association between obesity and vitD deficiency describing the main molecular mechanism of the relationship and the link with genetic factors. Key Messages: Low serum 25(OH)-D is positively associated with obesity or BMI in adults and children. Circulating vitD concentrations are, at least, partially determined by genetic factors. VitD plays an important role in the adipogenesis process and inflammation status in adipocytes and adipose tissue.

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“…These unexpected results may be due to a combination of differences in genetic susceptibility and environmental factors, both of which are implicated in MS causation. For example, previous studies have reported that environmental factors such as deficiency of vitamin D, Epstein Barr Virus infection and smoking may increase the risk of MS in genetically predisposed patients (3,4,5) as well as influence the expression levels of miR-155 and miR-146a (45)(46)(47) and consequently impacting the activity, disability and subtype of patients (43,44). Therefore, other functional polymorphisms of miR-155 and miR-146a genes should also be investigated to determine their association with susceptibility to MS.…”

Section: Age Of Onset Yearsmentioning

confidence: 99%

Relationship between miR‑155 and miR‑146a polymorphisms and susceptibility to multiple sclerosis in an Egyptian cohort

et al. 2020

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Multiple sclerosis (MS) is an autoimmune disorder of the central nervous system. It was previously demonstrated that miR-155 and miR-146a served a vital role in the pathophysiology of MS, and single nucleotide polymorphisms in miR-155 and miR-146a were found to be associated with the susceptibility to different autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis and type I diabetes. The aim of the present study was to analyze the association between susceptibility to MS and two genetic polymorphisms (miR-155 rs767649 A>T and miR-146a rs57095329 A>G) in a cohort of Egyptian patients. The presence of the two polymorphisms were analyzed in 114 patients with MS and 152 healthy controls using quantitative PCR. The present study demonstrated for the first time that: The TT genotype and T allele in miR-155 (rs767649 A>T) polymorphism were associated with an increased risk of MS; the miR-146a (rs57095329 A>G) mutated G allele conferred protection against the development of MS in all genetic models; miR-155 rs767649 A>T was a risk associated polymorphism of MS in females, but not in males; and miR-155 rs767649 AT/TT and miR-146a rs57095329 GG genotypes showed significantly higher distributions among patients with higher Expanded Disability Status Scale scores and secondary progressive MS subgroups. Therefore, miR-155 rs767649 polymorphism may confer susceptibility to MS, whereas miR-146a rs57095329 may be protective against MS in an Egyptian cohort.

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Vitamin D limits inflammation-linked microRNA expression in adipocytes in vitro and in vivo: A new mechanism for the regulation of inflammation by vitamin D

Cited by 88 publications

References 46 publications

Vitamin D Deficiency in Rats Causes Cardiac Dysfunction by Inducing Myocardial Insulin Resistance

Vitamin D Deficiency in Rats Causes Cardiac Dysfunction by Inducing Myocardial Insulin Resistance

Genetic Factors and Molecular Mechanisms of Vitamin D and Obesity Relationship

Relationship between miR‑155 and miR‑146a polymorphisms and susceptibility to multiple sclerosis in an Egyptian cohort

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