作者: Yuki Tanaka , Shinji Kume , Shin-ichi Araki , Keiji Isshiki , Masami Chin-Kanasaki
DOI: 10.1038/KI.2010.530
关键词: Kidney 、 Lipolysis 、 Lipotoxicity 、 Internal medicine 、 Kidney disease 、 Nephrology 、 Kidney metabolism 、 Medicine 、 Fenofibrate 、 Endocrinology 、 Fibrosis
摘要: As renal lipotoxicity can lead to chronic kidney disease (CKD), we examined the role of peroxisome proliferator-activated receptor (PPAR)-α, a positive regulator lipolysis. Feeding mice high-fat diet induced glomerular injury, and treating them with fenofibrate, PPARα agonist, increased expression lipolytic enzymes reduced lipid accumulation oxidative stress in glomeruli, while inhibiting development albuminuria fibrosis. In given an overload free fatty acid-bound albumin induce tubulointerstitial fenofibrate attenuated stress, macrophage infiltration, fibrosis, enhanced lipolysis interstitium. Fenofibrate inhibited palmitate-induced profibrotic plasminogen activator inhibitor-1 (PAI-1) cultured mesangial cells, both monocyte chemoattractant protein-1 PAI-1 proximal tubular cells along overexpression enzymes. Thus, attenuate lipotoxicity-induced injuries, enhancement Whether amelioration by agonists will turn out be useful strategy against CKD require direct testing.