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高脂肪高糖饮食补充维生素 D 可改善 LDLR 和 LDLR 小鼠的糖尿病前期表型。

Vitamin D supplementation of a high fat high sugar diet ameliorates prediabetic phenotype in female LDLR and LDLR mice.

机构信息

Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, UK.

College of Nursing, University of Raparin, Kurdistan Region, Iraq.

出版信息

Immun Inflamm Dis. 2017 Jun;5(2):151-162. doi: 10.1002/iid3.154. Epub 2017 Mar 13.

DOI:10.1002/iid3.154
PMID:28474500
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5418139/
Abstract

INTRODUCTION

Fatty liver disease is prevalent in populations with high caloric intake. Nutritherapeutic approaches are being considered, such as supplementary Vitamin D , 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 D , 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 D , as were systemic markers of inflammation (serum endotoxin and IL-6). M2 macrophage phenotype predominated in the group supplemented with additional Vitamin D . Beneficial changes were observed as early as five weeks' supplementation with Vitamin D and extended to restoration of high fat high sugar diet induced decrease of bone mineral density.

CONCLUSION

In summary, Vitamin D was a significantly beneficial dietary additive to blunt a prediabetic phenotype in diet-induced obesity of female LDLR and LDLR mice.

摘要

简介

脂肪肝疾病在高热量摄入的人群中普遍存在。人们正在考虑营养治疗方法,如补充维生素 D,以改善代谢综合征的各个方面,即脂肪肝疾病、高脂血症和与肥胖相关的胰岛素抵抗。

方法

我们分析了 LDLR 和 LDLR 雌性小鼠在 10 周致糖尿病饮食下的脂肪肝疾病、代谢应激和炎症标志物。

结果

与单独高脂肪高糖饮食组相比,补充维生素 D 的高脂肪高糖饮食组的转氨酶水平改善,明显较少出现高甘油三酯血症和高胰岛素血症,组织学上肝中心周围脂肪变性也较少。补充额外维生素 D 的组中非酯化脂肪酸和脂质过氧化产物的水平显著降低,全身性炎症标志物(血清内毒素和 IL-6)也是如此。补充额外维生素 D 的组中 M2 巨噬细胞表型占主导地位。早在补充维生素 D 五周后就观察到有益的变化,并扩展到恢复高脂肪高糖饮食诱导的骨密度降低。

结论

总之,维生素 D 是一种显著有益的饮食添加剂,可以减轻 LDLR 和 LDLR 雌性小鼠饮食诱导肥胖的糖尿病前期表型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4c/5418139/63c09bbb3a2d/IID3-5-151-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4c/5418139/fc70dd3c14a3/IID3-5-151-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4c/5418139/1057b089d540/IID3-5-151-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4c/5418139/08941a026751/IID3-5-151-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4c/5418139/b1faa56d994e/IID3-5-151-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4c/5418139/63c09bbb3a2d/IID3-5-151-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4c/5418139/fc70dd3c14a3/IID3-5-151-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4c/5418139/1057b089d540/IID3-5-151-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4c/5418139/08941a026751/IID3-5-151-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4c/5418139/b1faa56d994e/IID3-5-151-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4c/5418139/63c09bbb3a2d/IID3-5-151-g006.jpg

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