Role of 1,25-dihydroxyvitamin D3 in alleviating hepatic steatosis: Targeting M1 macrophage polarization in non-alcoholic fatty liver disease

Abstract

Non-alcoholic fatty liver disease (NAFLD), a critical global health concern, continues to challenge medical researchers with limited treatment options. This letter examines on the study by Luo et al, demonstrating that vitamin D 1,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃] improves hepatic steatosis in NAFLD by inhibiting M1 macrophage polarization via the vitamin D receptor-peroxisome proliferator-activated receptor gamma signaling pathway. This letter critically appraises these findings, comparing them to similar studies, and discusses their potential implications for treating NAFLD. Furthermore, we highlight future directions, including dose optimization and mechanistic studies.

Keywords: Vitamin D; Non-alcoholic fatty liver disease; M1 macrophage polarization; Vitamin D receptor pathway; Hepatic steatosis

Core Tip: This letter critically analyzes the study by Luo et al, on the effects of 1,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃] in reducing lipid accumulation in hepatocytes by inhibiting M1 macrophage polarization through the vitamin D receptor-peroxisome proliferator-activated receptor gamma pathway in non-alcoholic fatty liver disease (NAFLD). The study highlights how 1,25(OH)₂D₃ improves lipid metabolism and reduces inflammation, offering promising insights for NAFLD treatment. Future research should focus on dose optimization, detailed molecular mechanisms, and translating findings into human clinical trials to validate vitamin D's therapeutic potential in managing NAFLD.