维生素D对糖尿病大鼠肝脏脂质代谢和炎症的调节作用

Lipid metabolism and inflammation modulated by Vitamin D in liver of diabetic rats.

作者信息

Ning Conghua, Liu Lina, Lv Guodong, Yang Ye, Zhang Yuanyuan, Yu Rui, Wang Yongtao, Zhu Jun

机构信息

Department of Endocrinolog, First Affiliated Hospital of Xinjiang Medical University, No. 137 Liyushannan Road, Urumqi, 830054, Xinjiang, China.

Institute of Research, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, Xinjiang, China.

出版信息

Lipids Health Dis. 2015 Apr 18;14:31. doi: 10.1186/s12944-015-0030-5.

BACKGROUND

In recent years, much evidence suggested that vitamin D plays an important role in decreasing the risk of type 2 diabetes. The purpose of this study was to investigate whether 1, 25 (OH) 2D3 can modulate inflammation and lipid metabolism in type 2 diabetic rat liver.

METHODS

Type 2 diabetes was induced in SD rat with high-fat and high-sugar diets and multiple low-dose streptozotocin. The levels of serum calcium, phosphorus, glucose, TC, TG, AST, ALT and hepatic TG were determined. H & E staining were performed to assess the effects of vitamin D treatment on pathological changes in the liver tissues. Immunohistology, real-time PCR and Western blot were used to evaluate the expressions of NF-κ B, MCP-1, ICAM-1, TGF-β1, PPAR-α and CPT-1.

RESULTS

The administration of 1, 25 (OH) 2D3 reduced liver weight. Compared to DM rats, 1, 25 (OH) 2D3-treated DM rats had lower liver weight. Moreover, compared to healthy or 1, 25 (OH) 2D3-treated DM rats, DM rats had increased hepatic transcription factors (NF-κ B), monocyte chemoattractant protein -1 (MCP-1), intercellular adhesion molecule -1 (ICAM-1), transforming growth factor-β1 (TGF-β1) expressions, but had fewer hepatic PPAR- α and CPT-1 expressions.

CONCLUSIONS

1, 25 (OH) 2D3 significantly modulated the liver inflammation and lipid metabolism in diabetic rat models, which may be caused by its regulations on hepatic signaling NF-κ B pathway and PPAR- α.

背景

近年来，大量证据表明维生素D在降低2型糖尿病风险中发挥重要作用。本研究旨在探讨1,25(OH)₂D₃是否能调节2型糖尿病大鼠肝脏的炎症和脂质代谢。

方法

采用高脂高糖饮食联合多次低剂量链脲佐菌素诱导SD大鼠患2型糖尿病。测定血清钙、磷、葡萄糖、总胆固醇（TC）、甘油三酯（TG）、天冬氨酸转氨酶（AST）、丙氨酸转氨酶（ALT）及肝脏TG水平。进行苏木精-伊红（H&E）染色以评估维生素D治疗对肝组织病理变化的影响。采用免疫组织化学、实时荧光定量聚合酶链反应（real-time PCR）和蛋白质免疫印迹法（Western blot）评估核因子κB（NF-κB）、单核细胞趋化蛋白-1（MCP-1）、细胞间黏附分子-1（ICAM-1）、转化生长因子-β1（TGF-β1）、过氧化物酶体增殖物激活受体-α（PPAR-α）和肉碱/有机阳离子转运体-1（CPT-1）的表达。

结果

给予1,25(OH)₂D₃可减轻肝脏重量。与糖尿病（DM）大鼠相比，经1,25(OH)₂D₃治疗的DM大鼠肝脏重量更低。此外，与健康大鼠或经1,25(OH)₂D₃治疗的DM大鼠相比，DM大鼠肝脏转录因子（NF-κB）、单核细胞趋化蛋白-1（MCP-1）、细胞间黏附分子-1（ICAM-1）、转化生长因子-β1（TGF-β1）的表达增加，但肝脏PPAR-α和CPT-1的表达减少。