Muscle atrophy in chronic kidney disease results from abnormalities in insulin signaling

J Ren Nutr. 2010 Sep;20(5 Suppl):S24-8. doi: 10.1053/j.jrn.2010.05.007.

Abstract

Muscle atrophy is a significant consequence of chronic kidney disease that increases a patient's risk of mortality and decreases their quality of life. The loss of lean body mass results, in part, from an increase in the rate of muscle protein degradation. In this review, the proteolytic systems that are activated during chronic kidney disease and the key insulin signaling pathways that regulate the protein degradative processes are described.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Acidosis / complications
  • Animals
  • Chronic Disease
  • Glucocorticoids / biosynthesis
  • Humans
  • Insulin / physiology*
  • Insulin Resistance
  • Insulin-Like Growth Factor I / metabolism
  • Kidney Diseases / complications*
  • Muscle Proteins / metabolism
  • Muscular Atrophy / etiology*
  • Peptide Hydrolases / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction*

Substances

  • Glucocorticoids
  • Insulin
  • Muscle Proteins
  • Insulin-Like Growth Factor I
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt
  • Peptide Hydrolases