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Nephrol Dial Transplant. 2013 Nov;28 Suppl 4:iv29-36. doi: 10.1093/ndt/gft229. Epub 2013 Jul 30.

Autophagy and metabolic changes in obesity-related chronic kidney disease.

Author information

1
Division of Nephrology-Hypertension and O'Brien Kidney Center, Center for Renal Translational Medicine, Stein Institute for Research on Aging, University of California San Diego and the Veterans Administration San Diego Healthcare System, La Jolla, CA, USA.

Abstract

Obesity is a long-term source of cellular stress that predisposes to chronic kidney disease (CKD). Autophagy is a homeostatic mechanism for cellular quality control through the disposal and recycling of cellular components. During times of cellular stress, autophagy affords mechanisms to manage stress by selectively ridding the cell of the accumulation of potentially toxic proteins, lipids and organelles. The adaptive processes employed may vary between cell types and selectively adjust to the insult by inducing components of the basic autophagy machinery utilized by the cells while not under duress. In this review, we will discuss the autophagic responses of organs to cellular stressors, such as high-fat diet, obesity and diabetes, and how these mechanisms may prevent or promote the progression of disease. The identification of early cellular mechanisms in the advent of obesity- and diabetes-related renal complications could afford avenues for future therapeutic interventions.

KEYWORDS:

AMPK; diabetes; high fat diet; insulin resistance; mTOR

PMID:
23901047
PMCID:
PMC3814227
DOI:
10.1093/ndt/gft229
[Indexed for MEDLINE]
Free PMC Article
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