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Susceptibility of podocytes to palmitic acid is regulated by fatty acid oxidation and inversely depends on acetyl-CoA carboxylases 1 and 2.

Am J Physiol Renal Physiol.. 2014-02;  306(4):F401-F409
Kampe K, Sieber J, Orellana JM, Mundel P, Jehle AW. Dept. of Biomedicine, Molecular Nephrology, Rm. 303, Univ. Hospital Basel, Hebelstrasse 20, 4031 Basel, Switzerland.
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摘要

Type 2 diabetes is characterized by dyslipidemia with elevated free fatty acids (FFAs). Loss of podocytes is a hallmark of diabetic nephropathy, and podocytes are susceptible to saturated FFAs, which induce endoplasmic reticulum (ER) stress and podocyte death. Genome-wide association studies indicate that expression of acetyl-CoA carboxylase (ACC) 2, a key enzyme of fatty acid oxidation (FAO), is associated with proteinuria in type 2 diabetes. Here, we show that stimulation of FAO by aminoimidazole-4-carboxamide-1β-D-ribofuranoside (AICAR) or by adiponectin, activators of the low-energy sensor AMP-activated protein kinase (AMPK), protects from palmitic acid-induced podocyte death. Conversely, inhibition of... More

关键词

AMPK; apoptosis; diabetic nephropathy; palmitic acid; β-oxidation