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茯砖茶通过减轻骨骼肌胰岛素抵抗缓解高脂饮食诱导的大鼠慢性肾脏病。

Fu Brick Tea Alleviates Chronic Kidney Disease of Rats with High Fat Diet Consumption through Attenuating Insulin Resistance in Skeletal Muscle.

机构信息

Shaanxi Engineering Laboratory for Food Green Processing and Safety Control, and Shaanxi Key Laboratory for Hazard Factors Assessment in Processing and Storage of Agricultural Products, College of Food Engineering and Nutritional Science , Shaanxi Normal University , Xi'an 710119 , China.

出版信息

J Agric Food Chem. 2019 Mar 13;67(10):2839-2847. doi: 10.1021/acs.jafc.8b06927. Epub 2019 Mar 4.

DOI:10.1021/acs.jafc.8b06927
PMID:30829482
Abstract

Fu brick tea is a unique post-fermented dark tea product which undergoes controlled fermentation by "golden flower" fungus Eurotium cristatum. This study examined the effects of Fu brick tea aqueous extract (FTE) to alleviate insulin resistance, chronic kidney disease (CKD), and its regulatory mechanism in high fat diet (HFD)-induced obese rats. Sixteen-week administration of FTE at 400 mg/kg bw in rats significantly antagonized HFD-induced insulin resistance and CKD with elevations in serum leptin, TC, TG, LDL-C, blood urea nitrogen, uric acid, and creatinine levels, respectively ( p < 0.05). FTE treatment decreased the glomerular area, the thickness of basement membrane of renal tubules, and kidney fibrosis in HFD-fed rats. FTE alleviated insulin resistance through down-regulation of SIRP-α expression and activation of the insulin signaling Akt/GLUT4, FoxO1, and mTOR/S6K1 pathways in skeletal muscle. Furthermore, FTE prevented the HFD-caused kidney dysfunction and lipid or collagen accumulation, which was accompanied by the inhibition of GSK-3β phosphorylation and the action of PI3K/Akt and nuclear accumulation of Nrf2 in kidney. These results indicated that FTE alleviated insulin resistance and CKD through modulating insulin signal transduction cascades in skeletal muscle and enhanced the Nrf2 expression in kidney.

摘要

茯砖茶是一种独特的后发酵黑茶产品,经过“金花”真菌冠突散囊菌的控制发酵。本研究探讨了茯砖茶水提物(FTE)缓解高脂饮食(HFD)诱导肥胖大鼠胰岛素抵抗、慢性肾脏病(CKD)及其调节机制的作用。在大鼠中,400mg/kg bw 的 FTE 给药 16 周可显著拮抗 HFD 诱导的胰岛素抵抗和 CKD,血清瘦素、TC、TG、LDL-C、血尿素氮、尿酸和肌酐水平分别升高(p<0.05)。FTE 处理可降低 HFD 喂养大鼠的肾小球面积、肾小管基底膜厚度和肾脏纤维化。FTE 通过下调肌肉中 SIRP-α 的表达和激活胰岛素信号 Akt/GLUT4、FoxO1 和 mTOR/S6K1 通路来缓解胰岛素抵抗。此外,FTE 可防止 HFD 引起的肾功能障碍和脂质或胶原堆积,这伴随着 GSK-3β 磷酸化的抑制以及 PI3K/Akt 的作用和肾脏中 Nrf2 的核积累。这些结果表明,FTE 通过调节肌肉中的胰岛素信号转导级联来缓解胰岛素抵抗和 CKD,并增强肾脏中的 Nrf2 表达。

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