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1α,25(OH) 2 D 3 alleviates high glucose–induced lipid accumulation in rat renal tubular epithelial cells by inhibiting SREBPs
Author(s) -
Xu Miao,
Jiang Fei,
Li Bingyan,
Zhang Zengli
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28786
Subject(s) - lipid metabolism , diabetic nephropathy , sterol regulatory element binding protein , endocrinology , medicine , downregulation and upregulation , western blot , carbohydrate metabolism , chemistry , biology , biochemistry , diabetes mellitus , sterol , cholesterol , gene
Lipid accumulation is a vital event in the progression of diabetic nephropathy. 1,25‐Dihydroxyvitamin D3 (1α,25(OH) 2 D 3 ) is considered to have a protective effect on diabetic nephropathy. However, it remains unclear whether 1α,25(OH) 2 D 3 can inhibit lipid accumulation, and the potential mechanisms responsible for lipid metabolism are incompletely understood. In this study, we evaluated the effects of 1α,25(OH) 2 D 3 on lipid metabolism in high glucose–exposed rat renal tubular epithelial NRK‐52E cells. Results indicated that high glucose–enhanced lipid accumulation in NRK‐52E cells and 1α,25(OH) 2 D 3 can remarkably decrease high glucose–induced lipid accumulation. Western blot showed that 1α,25(OH) 2 D 3 alleviated high glucose–induced upregulation of sterol regulatory element‐binding protein‐1c (SREBP‐1c) and SREBP2, along with their established target genes fatty acid synthase (FASN) and hydroxymethylglutaryl CoA reductases (HMGCR). Overall, these findings suggest that 1α,25(OH) 2 D 3 downregulated the expressions of SREBPs to inhibit high glucose–induced lipid accumulation, which provides new sights into the protective effects of 1α,25(OH) 2 D 3 on diabetic nephropathy.