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目的:研究黄连素(BBR)对肥胖2型糖尿病(OT2DM)中国地鼠内脏白色脂肪组织(VWAT)中受体相互作用蛋白140(Receptor-interacting protein 140,RIP140)/PR结构域蛋白16(PR domain containing 16,PRDM16)信号通路基因mRNA表达的影响及相关机制。方法:以高脂饮食诱导肥胖胰岛素抵抗(OIR)地鼠模型,然后给予小剂量链脲菌素(STZ)建立OT2DM地鼠模型。造模完成后随机分成对照组、OIR组、OT2DM组和OT2DM BBR治疗组。BBR治疗9周,应用real-time RT-PCR技术检测各组地鼠VWAT中RIP140/PRDM16信号通路基因mRNA表达改变。结果:模型地鼠VWAT中RIP140、PKCε、PRMT1、Exportin1和白脂组织特异基因Resistin和Serpina3k的mRNA表达增加,而PRDM16、CtBP-1、CtBP-2、C/EBPβ、PPARγ、PGC-1α、PGC-1β、Gyk、GPDH、AQP7、GLUT4及棕脂组织特异基因UCP-1、Cidea、Elovl3和PPARα的mRNA表达降低。BBR治疗抑制VWAT中RIP140调控通路,诱导PRDM16信号通路,诱导棕脂组织特异基因mRNA的表达,抑制白色脂肪选择性基因的表达,诱导VWAT棕色化,改善脂诱性胰岛素抵抗(FIIR)。结论:RIP140/PRDM16信号通路参与BBR诱导VWAT棕色化的分子机制。
OBJECTIVE: To investigate the effects of berberine (BBR) on the expression of RIP140 / PR domain protein 16 (PR) in obese type 2 diabetic (OT2DM) Chinese hamster visceral white adipose tissue (VWAT) domain containing 16, PRDM16) mRNA expression and related mechanisms. Methods: The model of obese insulin resistance (OIR) was induced by a high-fat diet, and then a small dose of streptozotocin (STZ) was given to establish the OT2DM hamster model. After modeling, they were randomly divided into control group, OIR group, OT2DM group and OT2DM BBR treatment group. BBR treatment for 9 weeks, real-time RT-PCR technique was used to detect the change of RIP140 / PRDM16 signal pathway mRNA expression in VWAT of each group. Results: The mRNA expressions of RIP140, PKCε, PRMT1, Exportin1 and white adipose tissue-specific genes Resistin and Serpina3k increased in model hamster VWAT, while the expressions of PRDM16, CtBP-1, CtBP-2, C / EBPβ, PPARγ, PGC- -1β, Gyk, GPDH, AQP7, GLUT4 and the mRNA expressions of UCP-1, Cidea, Elovl3 and PPARα in the palm fat tissue. BBR treatment inhibited RIP140 regulatory pathway in VWAT, induced PRDM16 signaling, induced the expression of brown fat-specific gene mRNA, inhibited the expression of white fat-selective genes, induced the browning of VWAT, and improved the lipid-induced insulin resistance (FIIR). Conclusion: RIP140 / PRDM16 signaling pathway is involved in BBR-induced molecular mechanism of VWAT browning.