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首页> 外文期刊>Journal of diabetes. >Renoprotective effects of brown adipose tissue activation in diabetic mice
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Renoprotective effects of brown adipose tissue activation in diabetic mice

机译：Renoprotective褐色脂肪组织的影响激活在糖尿病小鼠

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Abstract Background Brown adipose tissue (BAT) has been regarded as a potential target organ to combat obesity and related metabolic disorders. However, the effect of BAT activation on the development of diabetic kidney disease (DKD) remains unclear. Methods Diabetic mice were induced by streptozotocin (STZ) combined with a high‐fat diet. To activate BAT, mice were administered 1 mg/kg per day, i.p., CL316,243, a β 3 ‐adrenergic receptor agonist, for 4 weeks. Blood glucose, serum lipids, adipokines, 24‐hour urinary albumin, 8‐hydroxydeoxyguanosine (8‐OHdG), and circulating microRNA (miRNA) levels were analyzed, in addition to renal pathology. Histological changes (fibrosis, inflammation) were evaluated in the kidneys, as was the expression of oxidative stress‐related genes. Renal signaling pathways (fibroblast growth factor [Fgf]21/β‐klotho/FGF receptor 1c and AMP‐activated protein kinase[AMPK]/sirtuin 1 [Sirt1]/peroxisome proliferator‐activated receptor‐γ coactivator‐1α [Pgc1α]) were also evaluated. Results Compared with untreated STZ‐diabetic mice, CL316,243 treatment reduced blood glucose, albeit not significantly (20.58?±?3.55 vs 23.60?±?3.90 mM), and significantly decreased triglycerides and low‐density lipoprotein cholesterol and increased high‐density lipoprotein cholesterol. Simultaneously, BAT activation significantly decreased 24‐hour urinary albumin (34.21?±?6.28 vs 70.46?±?15.81?μg/24?h; P ??0.05) and 8‐OHdG, improved renal fibrosis, inflammation, and oxidative stress, and ameliorated renal morphological abnormalities. In addition to enhancing BAT activity, CL316,243 significantly increased serum adiponectin concentrations and renal Fgf21 sensitivity, and reactivated the renal AMPK/Sirt1/Pgc1α signaling pathway. Furthermore, CL316,243 treatment increased levels of some circulating miRNAs and downregulated expression of their target genes in the kidney. Conclusions Activating BAT could improve kidney injury in diabetic mice via metabolic improvements and renal AMPK activation by beneficial adipokines and miRNAs.
机译：抽象背景褐色脂肪组织(蝙蝠)被认为是一个潜在的靶器官对抗肥胖和代谢紊乱有关。然而,蝙蝠的激活的影响糖尿病肾病的发展(DKD)仍不清楚。由链脲霉素(STZ)结合高脂肪的饮食。管理1毫克/公斤/天,i.p CL316,243,β3肾上腺素能受体激动剂,应承担的4周。血糖、血清脂质、发病24小时尿白蛋白8 hydroxydeoxyguanosine高OHdG区域(8)和循环微rna (microRNA)水平分析了,除了肾脏病理。组织学变化(纤维化炎症)在肾脏进行评估,是吗表达式的氧化应激相关基因。肾信号通路(纤维母细胞生长地理因素(Fgf) 21 /β克罗索/ Fgf受体1 cAMP激活的蛋白激酶(AMPK)应承担/ sirtuin蛋白1[Sirt1] /过氧物酶体扩散国的激活地理地理受体γ共激活剂1α[Pgc1α])也评估。STZ所致糖尿病小鼠,CL316,243治疗减少了血糖,尽管不明显(3.55 vs 23.60±20.58 ? ?±3.90毫米),和显著降低甘油三酯和低密度脂蛋白胆固醇和增加高密度脂蛋白胆固醇。同时,蝙蝠显著激活24小时尿白蛋白应承担的下降(6.28±34.21 ?15.81 vs 70.46±? ?μg / 24 ? h;8高OHdG改善肾纤维化炎症,和氧化压力,改善肾功能形态学异常。显著提高蝙蝠活动,CL316,243血清脂联素浓度和增加肾Fgf21敏感性,并重新激活肾AMPK / Sirt1 Pgc1α信号通路。此外,CL316,243治疗水平上升一些流传的microrna表达下调他们的目标基因的表达在肾脏。结论激活蝙蝠可以改善肾脏通过代谢损伤在糖尿病小鼠改进和肾AMPK活化有益的发病和microrna。

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