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      Adipokines as uremic toxins.

      Journal of renal nutrition : the official journal of the Council on Renal Nutrition of the National Kidney Foundation
      Adipokines, blood, physiology, toxicity, Adiponectin, Adipose Tissue, physiopathology, Drug-Related Side Effects and Adverse Reactions, Humans, Inflammation, Leptin, Nicotinamide Phosphoribosyltransferase, Obesity, complications, Oxidative Stress, Resistin, Signal Transduction, Uremia, metabolism

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          Abstract

          The adipose tissue has pleiotropic functions far beyond the mere storage of energy, and it secretes a number of hormones and cytokines, called adipokines, which have biological effects that impact heath and disease. Adipokines are markedly elevated in the plasma of uremic patients, mainly due to decreased renal excretion. They have pluripotent signaling effects on inflammation/oxidative stress (leptin, adiponectin, resistin), protein-energy wasting (leptin, adiponectin), insulin signaling (adiponectin, leptin, visfatin), endothelial dysfunction (visfatin), and vascular damage (adiponectin, leptin, resistin), which are prevalent in uremic patients. Obesity superimposed to uremia may further aggravate hyperadipokinemia, with the exception of adiponectinemia, which is mitigated by adiposity. Among adipokines and until more data become available, only leptin may be considered as a full uremic toxin owing to adverse effects on protein-energy wasting, cardiovascular damage, inflammation, and the immune system, which have been documented both clinically and experimentally. Resistin and visfatin display some features of uremic toxins, but more data are needed to consider these adipokines as true uremic toxins. In contrast, high levels of adiponectin and chemerin seen in uremia appear to be beneficial. Further research is needed to investigate whether selective removal of leptin, resistin, and visfatin and increments of adiponectin and chemerin levels may have clinical relevance in uremic patients. Copyright © 2012 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.

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