Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/40075
Title: Vitamin D3 supplementation of a high fat high sugar diet ameliorates prediabetic phenotype in female LDLR(-/-) and LDLR(+/+) mice
Authors: Kheder, Ramiar
Hobkirk, James
Saeed, Zeayd
Janus, Justyna
Carroll, Sean
Browning, Michael J.
Stover, Cordula
First Published: 13-Mar-2017
Publisher: Wiley
Citation: Immun Inflamm Dis, 2017, 5 (2), pp. 151-162
Abstract: INTRODUCTION: Fatty liver disease is prevalent in populations with high caloric intake. Nutritherapeutic approaches are being considered, such as supplementary Vitamin D3 , to improve aspects of metabolic syndrome, namely fatty liver disease, hyperlipidemia, and insulin resistance associated with obesity. METHODS: We analyzed female LDLR(-/-) and LDLR(+/+) mice on a 10-week diabetogenic diet for markers of fatty liver disease, metabolic strain, and inflammation. RESULTS: The groups on a high fat high sugar diet with supplementary Vitamin D3 , in comparison with the groups on a high fat high sugar diet alone, showed improved transaminase levels, significantly less hypertriglyceridemia and hyperinsulinemia, and histologically, there was less pericentral hepatic steatosis. Levels of non-esterified fatty acids and lipid peroxidation products were significantly lower in the group supplemented with additional Vitamin D3 , as were systemic markers of inflammation (serum endotoxin and IL-6). M2 macrophage phenotype predominated in the group supplemented with additional Vitamin D3 . Beneficial changes were observed as early as five weeks' supplementation with Vitamin D3 and extended to restoration of high fat high sugar diet induced decrease of bone mineral density. CONCLUSION: In summary, Vitamin D3 was a significantly beneficial dietary additive to blunt a prediabetic phenotype in diet-induced obesity of female LDLR(-/-) and LDLR(+/+) mice.
DOI Link: 10.1002/iid3.154
eISSN: 2050-4527
Links: http://onlinelibrary.wiley.com/doi/10.1002/iid3.154/abstract
http://hdl.handle.net/2381/40075
Version: Publisher Version
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright © the authors, 2017. This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Appears in Collections:Published Articles, Dept. of Infection, Immunity and Inflammation

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