Molecular nutrition & food research · 2019
Vitamin D Deficiency in Rats Causes Cardiac Dysfunction by Inducing Myocardial Insulin Resistance.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Nizami Hina Lateef, Katare Parmeshwar, Prabhakar Pankaj, Kumar Yashwant, Arava Sudheer Kumar, Chakraborty Praloy, Maulik Subir Kumar, Banerjee Sanjay Kumar
Аннотация
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.
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.