Kim Yoon-Ah, Oh Minha, Jung Sohee, Kwon Deok Hoon, Lee Ga Young, Han Sung Nim
Department of Food and Nutrition, College of Human Ecology, Seoul National University, Seoul, Korea.
Department of Food and Nutrition, College of Human Ecology, Seoul National University, Seoul, Korea; Research Institute of Human Ecology, Seoul National University, Seoul, Korea.
J Nutr Biochem. 2025 Nov;145:110037. doi: 10.1016/j.jnutbio.2025.110037. Epub 2025 Jul 16.
Type 2 diabetes is characterized by chronic low-grade inflammation and insulin resistance resulting from activation and infiltration of immune cells into adipose tissue. Vitamin D reportedly exerts an anti-inflammatory effect by regulating immune cell activity and inflammatory cytokine production. This study aimed to investigate the effects of vitamin D supplementation on lymphoid and myeloid immune cell distribution in the adipose tissue and explore the mechanisms by which vitamin D modulates adipose tissue inflammation in diabetes. Five-week-old, male C57BLKS/J-m/m (CON) and C57BLKS/J-db/db (DB) mice were fed diets containing either 1,000 or 10,000 IU vitamin D/kg diet for 8 weeks. Vitamin D supplementation resulted in a smaller weight gain (33.8% lower), less adipocyte hypertrophy (16.9% lower), and a lower fasting blood glucose concentration (7.4% lower) in DB group. Vitamin D supplementation did not inhibit macrophage and dendritic cell infiltration into adipose tissue; nonetheless, it reduced the percentage of CD8 T cells (18% lower). In DB group, vitamin D supplementation downregulated the gene expression of interleukin 6 (Il6) and CC motif chemokine ligand 2 (Ccl2) in stromal vascular cells (28.2% and 17.3% lower, respectively) as well as that of Il6, Ccl2, sterol regulatory element-binding transcription factor 1 (Srebf1), and advanced glycosylation end product-specific receptor (Ager) in adipose tissue (42.8%, 24.9%, 33.1%, and 58.2% lower, respectively). In conclusion, vitamin D supplementation attenuated the inflammatory response and adipocyte hypertrophy in adipose tissue from diabetic mice. The inhibition of Ager and Srebf1 by vitamin D supplementation potentially contributes to vitamin D's anti-inflammatory and anti-adiposity effects in diabetic mice.
2型糖尿病的特征是慢性低度炎症以及免疫细胞激活并浸润到脂肪组织中导致的胰岛素抵抗。据报道，维生素D通过调节免疫细胞活性和炎性细胞因子产生发挥抗炎作用。本研究旨在探讨补充维生素D对脂肪组织中淋巴细胞和髓样免疫细胞分布的影响，并探索维生素D调节糖尿病患者脂肪组织炎症的机制。给5周龄雄性C57BLKS/J-m/m（对照）和C57BLKS/J-db/db（糖尿病）小鼠喂食含1000或10000 IU维生素D/kg饲料的日粮，持续8周。补充维生素D使糖尿病组小鼠体重增加幅度更小（降低33.8%）、脂肪细胞肥大程度减轻（降低16.9%）、空腹血糖浓度降低（降低7.4%）。补充维生素D并未抑制巨噬细胞和树突状细胞浸润到脂肪组织中；尽管如此，它降低了CD8 T细胞的百分比（降低18%）。在糖尿病组中，补充维生素D下调了基质血管细胞中白细胞介素6（Il6）和CC基序趋化因子配体2（Ccl2）的基因表达（分别降低28.2%和17.3%）以及脂肪组织中Il6、Ccl2、固醇调节元件结合转录因子1（Srebf1）和晚期糖基化终产物特异性受体（Ager）的基因表达（分别降低42.8%、24.9%、33.1%和58.2%）。总之，补充维生素D减轻了糖尿病小鼠脂肪组织中的炎症反应和脂肪细胞肥大。补充维生素D对Ager和Srebf1的抑制作用可能有助于其在糖尿病小鼠中的抗炎和抗肥胖作用。
