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However, it remains unclear whether 1\u03b1,25(OH)<jats:sub>2<\/jats:sub>D<jats:sub>3<\/jats:sub> can inhibit lipid accumulation, and the potential mechanisms responsible for lipid metabolism are incompletely understood. In this study, we evaluated the effects of 1\u03b1,25(OH)<jats:sub>2<\/jats:sub>D<jats:sub>3<\/jats:sub> on lipid metabolism in high glucose\u2013exposed rat renal tubular epithelial NRK\u201052E cells. Results indicated that high glucose\u2013enhanced lipid accumulation in NRK\u201052E cells and 1\u03b1,25(OH)<jats:sub>2<\/jats:sub>D<jats:sub>3<\/jats:sub> can remarkably decrease high glucose\u2013induced lipid accumulation. Western blot showed that 1\u03b1,25(OH)<jats:sub>2<\/jats:sub>D<jats:sub>3<\/jats:sub> alleviated high glucose\u2013induced upregulation of sterol regulatory element\u2010binding protein\u20101c (SREBP\u20101c) and SREBP2, along with their established target genes fatty acid synthase (FASN) and hydroxymethylglutaryl CoA reductases (HMGCR). Overall, these findings suggest that 1\u03b1,25(OH)<jats:sub>2<\/jats:sub>D<jats:sub>3<\/jats:sub> downregulated the expressions of SREBPs to inhibit high glucose\u2013induced lipid accumulation, which provides new sights into the protective effects of 1\u03b1,25(OH)<jats:sub>2<\/jats:sub>D<jats:sub>3<\/jats:sub> on diabetic nephropathy.<\/jats:p>","DOI":"10.1002\/jcb.28786","type":"journal-article","created":{"date-parts":[[2019,4,25]],"date-time":"2019-04-25T06:35:20Z","timestamp":1556174120000},"page":"15211-15221","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["1\u03b1,25(OH)<sub>2<\/sub>D<sub>3<\/sub> alleviates high glucose\u2013induced lipid accumulation in rat renal tubular epithelial cells by inhibiting 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