Muscle atrophy in chronic kidney disease results from abnormalities in insulin signaling.
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.
Price
S Russ
SR
Renal Division, School of Medicine, Emory University, Atlanta, Georgia 30322, USA. russ.price@emory.edu
Gooch
Jennifer L
JL
Donaldson
Sue K
SK
Roberts-Wilson
Tiffany K
TK
D000138:Acidosis / Q000150:complications; D000818:Animals; D002908:Chronic Disease; D005938:Glucocorticoids / Q000096:biosynthesis; D006801:Humans; D007328:Insulin / Q000502:physiology*; D007333:Insulin Resistance; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D007674:Kidney Diseases / Q000150:complications*; D009124:Muscle Proteins / Q000378:metabolism; D009133:Muscular Atrophy / Q000209:etiology*; D010447:Peptide Hydrolases / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D015398:Signal Transduction
D005938:Glucocorticoids; D007328:Insulin; D009124:Muscle Proteins; D007334:Insulin-Like Growth Factor I; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D010447:Peptide Hydrolases
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