Delayed treatment with fenofibrate protects against high-fat diet-induced kidney injury in mice: the possible role of AMPK-autophagy.

Delayed treatment with fenofibrate protects against high-fat diet-induced kidney injury in mice: the possible role of AMPK-autophagy. Am J Physiol Renal Physiol. 2016 Jul 27;:ajprenal.00596.2015 Authors: Sohn M, Kim K, Uddin MJ, Lee G, Hwang I, Kang H, Kim H, Lee JH, Ha H Abstract Fenofibrate activates not only peroxisome proliferator-activated receptor α (PPARα) but also adenosine monophosphate-activated protein kinase (AMPK). AMPK-mediated cellular responses protect kidney from high-fat diet (HFD)-induced injury, and autophagy resulting from AMPK activation has been regarded as a stress-response mechanism. Thus, the present study examined the role of AMPK and autophagy in the renotherapeutic effects of fenofibrate. C57BL/6J mice were divided into 3 groups: normal diet (ND), HFD, and HFD+fenofibrate (HFD+FF). Fenofibrate was administered 4 weeks after the initiation of the HFD when renal injury was initiated. Mouse proximal tubule cells (mProx24) were used to clarify the role of AMPK. Feeding mice with HFD for 12 weeks induced insulin resistance and kidney injury such as albuminuria, glomerulosclerosis, tubular injury, and inflammation, which were effectively inhibited by fenofibrate. In addition, fenofibrate treatment resulted in the activation of renal AMPK, upregulation of fatty acid oxidation (FAO) enzymes and antioxidants, and induction of autophagy in the HFD mice. In mProx24 cells, fenofibrate activated AMPK in a concentration-depende...
Source: Am J Physiol Renal P... - Category: Urology & Nephrology Authors: Tags: Am J Physiol Renal Physiol Source Type: research

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