The role of nuclear receptors in the kidney in obesity and metabolic syndrome.

Genes Nutr

Department of Nephrology and Mineral Metabolism, National Medical Science and Nutrition Institute, Salvador Zubirán, Vasco de Quiroga No. 15, Tlalpan, 14000, Mexico, D.F., Mexico,

Published: October 2012

AI Article Synopsis

  • Nuclear receptors are crucial in regulating kidney functions and metabolic processes, impacting lipid metabolism, inflammation, and drug clearance.
  • Disruption of nuclear receptor activity, often linked to obesity, can lead to metabolic syndrome and exacerbate chronic kidney diseases, potentially ending in kidney failure.
  • The review highlights several specific nuclear receptors and their roles in kidney-related issues tied to obesity and metabolic syndrome, suggesting they could be targets for new treatments.

Article Abstract

Nuclear receptors are ligand-activated transcriptional regulators of several key aspects of renal physiology and pathophysiology. As such, nuclear receptors control a large variety of metabolic processes, including kidney lipid metabolism, drug clearance, inflammation, fibrosis, cell differentiation, and oxidative stress. Derangement of nuclear receptor regulation, that is, mainly due to obesity may induce metabolic syndrome, may contribute to the pathogenesis and progression of chronic renal disease and may result in end-stage renal disease. This places nuclear receptors at the forefront of novel therapeutic approaches for a broad range of kidney disorders and diseases, including glomerulosclerosis, tubulointerstitial disease, renal lipotoxicity, kidney fibrosis, and hypertension. This review focuses on the importance of the transcription factors peroxisome proliferator-activated receptor alpha, peroxisome proliferator-activated receptor beta, peroxisome proliferator-activated receptor gamma, liver X receptors, farnesoid X receptor, and the pregnane X receptor/steroid and xenobiotic receptor (PXR) on the physiology and pathophysiology of renal diseases associated with obesity and metabolic syndrome.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3448033PMC
http://dx.doi.org/10.1007/s12263-012-0295-5DOI Listing

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