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Title of Journal: Mol Cell Biochem

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Abbravation: Molecular and Cellular Biochemistry

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Springer US

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DOI

10.1007/s00391-007-0439-1

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1573-4919

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Manganese supplementation increases adiponectin an

Authors: Elodie Burlet Sushil K Jain
Publish Date: 2017/01/13
Volume: 429, Issue: 1-2, Pages: 1-10
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Abstract

Blood and tissue levels of manganese Mn are lower in type 2 diabetic and atherosclerosis patients compared with healthy subjects Adiponectin has antidiabetic and antiatherogenic properties Impairment in Disulfide bond Alike protein DsbAL is associated with low adiponectin levels and diabetes This study investigates the hypothesis that the beneficial effects of Mn supplementation are mediated by adiponectin and DsbAL At 6 weeks of age Male Zucker diabetic fatty rats ZDF were randomly divided into two groups diabetic controls and Mnsupplemented diabetic rats Each rat was supplemented with Mn D+Mn 16 mg/kg BW or water placebo D+P daily for 7 weeks by oral gavage For cell culture studies Human Umbilical Vein Endothelial Cells HUVEC or 3T3L1 adipocytes were pretreated with Mn 0–10 µM MnCl2 for 24 h followed by high glucose HG 25 mM or normal glucose 5 mM exposure for another 24 h Mn supplementation resulted in higher adiponectin p = 001 and lower ICAM1 p = 004 and lower creatinine p = 004 blood levels compared to those in control ZDF rats Mnsupplemented rats also caused reduced oxidative stress ROS and NADPH oxidase and higher DsbAL expression in the liver p = 003 of ZDF rats compared to those in livers of control rats however Fe levels in liver were lower but not significant p = 008 Similarly treatment with high glucose 25 mM caused a decrease in DsbAL which was prevented by Mn supplementation in HUVEC and adipocytes Mechanistic studies with DsbAL siRNA showed that the beneficial effects of Mn supplementation on ROS NOX4 and ICAM1 expression were abolished in DsbAL knockdown HUVEC These studies demonstrate that DsbALlinked adiponectin mediates the beneficial effects observed with Mn supplementation and provides evidence for a novel mechanism by which Mn supplementation can increase adiponectin and reduce the biomarkers of endothelial dysfunction in diabetesThe authors are supported by Grants from NCCIH and the Office of Dietary Supplements of the National Institutes of Health RO1 AT007442 the Malcolm Feist Endowed Chair in Diabetes and funded by a fellowship from the Malcolm Feist Cardiovascular Research Endowment LSU Health Shreveport The authors thank Ms Georgia Morgan for excellent editing of this manuscript

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