Effects of glucose homeostasis on protein metabolism in patients with advanced chronic kidney disease.
Insulin deficiency is known to be associated with a state of increased muscle protein breakdown; this process is mediated by the ubiquitin-proteasome pathway. Convincing in vitro data are further supported by extensive studies in humans with insulin deprivation and are further substantiated by reversal of muscle protein breakdown with insulin treatment. In patients with end-stage renal disease (ESRD) and diabetes mellitus (DM), muscle protein breakdown is enhanced in both acute and chronic conditions. Recent data also point to the potential protein catabolic effects of insulin resistance combined with insulin deficiency. Because ESRD is associated with a state of insulin resistance, uremic muscle wasting may also be mediated by this pathway.
Ikizler
T Alp
TA
Division of Nephrology, Vanderbilt University Medical Center, Nashville, TN 37232-2372, USA. alp.ikizler@Vanderbilt.Edu
D003920:Diabetes Mellitus / Q000378:metabolism; D005947:Glucose / Q000378:metabolism* / Q000502:physiology; D006706:Homeostasis; D006801:Humans; D007328:Insulin / Q000172:deficiency / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology; D007676:Kidney Failure, Chronic / Q000378:metabolism* / Q000628:therapy; D008660:Metabolism; D009752:Nutritional Status; D011506:Proteins / Q000378:metabolism*; D006435:Renal Dialysis; D014511:Uremia / Q000378:metabolism
D007328:Insulin; D011506:Proteins; D005947:Glucose