Obesity-Related Chronic Kidney Disease—The Role of Lipid Metabolism

Metabolites

Peter Mount¹  Matthew Davies¹  Suet-Wan Choy¹  Natasha Cook¹  David Power¹ 

[1] Department of Nephrology, Austin Health, Heidelberg, Melbourne 3084, Australia; E-Mails:

关键词: obesity;    chronic kidney disease;    lipid metabolism;    AMP-activated protein kinase;    acetyl-CoA carboxylase;    high fat diet;    podocyte;    mesangial cell;    proximal tubule;   

DOI  :  10.3390/metabo5040720

来源: mdpi

【 摘 要 】

Obesity is an independent risk factor for chronic kidney disease (CKD). The mechanisms linking obesity and CKD include systemic changes such as high blood pressure and hyperglycemia, and intrarenal effects relating to lipid accumulation. Normal lipid metabolism is integral to renal physiology and disturbances of renal lipid and energy metabolism are increasingly being linked with kidney disease. AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) are important regulators of fatty acid oxidation, which is frequently abnormal in the kidney with CKD. A high fat diet reduces renal AMPK activity, thereby contributing to reduced fatty acid oxidation and energy imbalance, and treatments to activate AMPK are beneficial in animal models of obesity-related CKD. Studies have found that the specific cell types affected by excessive lipid accumulation are proximal tubular cells, podocytes, and mesangial cells. Targeting disturbances of renal energy metabolism is a promising approach to addressing the current epidemic of obesity-related kidney disease.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.