Obesity‐induced chronic inflammation is a key component in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) and insulin resistance. Increased secretion of proinflammatory cytokines by macrophages in metabolic tissues promotes disease progression. In the diet‐induced obesity (DIO) mouse model, activation of liver resident macrophages, or Kupffer cells (KCs), drives inflammatory responses, which recruits circulating macrophages and promotes fatty liver development, and ultimately contributes to impaired hepatic insulin sensitivity. Hepatic macrophages express the highest level of vitamin D receptors (VDRs) among nonparenchymal cells, whereas VDR expression is very low in hepatocytes. VDR activation exerts anti‐inflammatory effects in immune cells.

中文翻译：

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肝脏巨噬细胞中维生素 D 受体的激活可改善小鼠的肝脏炎症、脂肪变性和胰岛素抵抗

肥胖引起的慢性炎症是非酒精性脂肪性肝病 (NAFLD) 和胰岛素抵抗发病机制的关键组成部分。代谢组织中巨噬细胞分泌促炎细胞因子增加促进疾病进展。在饮食诱导的肥胖 (DIO) 小鼠模型中，肝脏驻留巨噬细胞或库普弗细胞 (KCs) 的激活会驱动炎症反应，从而招募循环巨噬细胞并促进脂肪肝的发展，并最终导致肝脏胰岛素敏感性受损。肝巨噬细胞在非实质细胞中表达最高水平的维生素 D 受体 (VDR)，而在肝细胞中 VDR 表达非常低。VDR 激活在免疫细胞中发挥抗炎作用。