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Vitamin D Deficiency Attenuates Acute Alcohol‐Induced Hepatic Lipid Accumulation in Mice
Author(s) -
Hu ChunQiu,
Xu Meng,
Yang BingBing,
Liu XiaoJing,
Bo QingLi,
Zhang Cheng,
Xu DeXiang
Publication year - 2019
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1002/lipd.12188
Subject(s) - endocrinology , medicine , vitamin , fatty liver , steatosis , vitamin d deficiency , beta oxidation , lipid metabolism , fatty acid synthase , vitamin a deficiency , chemistry , biology , retinol , vitamin d and neurology , metabolism , disease
Vitamin D deficiency has been frequently reported in chronic liver disease. However, its influence on hepatic lipid accumulation in alcoholic liver disease remains unclear. The present study investigated the effects of vitamin D deficiency on acute alcohol‐induced hepatic lipid metabolism in mice. Mice were fed with vitamin D deficient diet, in which vitamin D was depleted for 12 weeks to establish an animal model of vitamin D deficiency. Some mice were administered a single gavage of alcohol (4 g/kg bodyweight) before they were euthanized. Results show that feeding mice with vitamin D deficient diet did not induce hepatic lipid accumulation. In contrast, vitamin D deficiency markedly reduced alcohol‐induced triacylglycerol (TAG) content and prevented hepatic lipid accumulation. Moreover, vitamin D deficiency significantly attenuated alcohol‐induced sterol‐regulated element‐binding protein (SREBP)‐1c activation, which regulates genes for hepatic fatty acid (FA) and TAG synthesis, and the expression of its target genes fatty acid synthase ( Fasn ) and acetyl‐coenzyme‐ A carboxylase ( Acc ). In addition, vitamin D deficiency alleviated alcohol‐induced downregulation of hepatic nuclear peroxisome proliferator‐activated receptor (PPAR)α, which governs FA transport and β‐oxidation, and the expression of Carnitine palmitoyltransferase ( Cpt )‐1α, cytochrome P450, family 4, subfamily a, polypeptide ( Cyp4a ) 10 , and Cyp4a14 , which are key enzymes for hepatic fatty acids β‐oxidation and ω‐oxidation. Taken together, these results suggest that vitamin D deficiency is not a direct risk factor for hepatic lipid accumulation. Vitamin D deficiency alleviates acute alcohol‐induced hepatic lipid accumulation through inhibiting hepatic de novo fatty acid syntheses and promoting fatty acid β‐oxidation and ω‐oxidation.