title: Insulin resistance and protein metabolism in chronic hemodialysis patients.
abstract: OBJECTIVE
  Loss of lean body mass (sarcopenia) is associated with increased morbidity and mortality in patients receiving chronic hemodialysis (CHD). Insulin resistance (IR), which is highly prevalent in patients receiving CHD, has been proposed to play a critical role in the development of sarcopenia. The aim of this study was to examine the effect of IR on amino acid metabolism in patients receiving CHD.
  
  
  METHODS
  This was a cross-sectional study.
  
  
  METHODS
  The study included 12 prevalent (i.e., patients that have been on dialysis for more than 90 days) African American patients receiving CHD.
  
  
  METHODS
  IR was measured as glucose disposal rate (GDR) determined from hyperinsulinemic euglycemic clamp (HGEC) studies performed 3 consecutive times. Plasma amino acid (AA) concentrations were measured by real-time high-performance liquid chromatography (HPLC) throughout the clamp study. The primary outcome was percentage change in leucine concentrations during the clamp study. The main predictor was the GDR measured simultaneously during the HGEC studies. Mixed model analysis was used to account for repeated measures.
  
  
  RESULTS
  All individual AA concentrations declined significantly in response to high-dose insulin administration (P < .001). There was a significant direct association between GDR by HECG studies and the percentage change in leucine concentration (P = .02). Although positive correlations were observed between GDR values and concentration changes from baseline for other AAs, these associations did not reach statistical significance.
  
  
  CONCLUSIONS
  Our results suggest that the severity of IR of carbohydrate metabolism is associated with a lesser decline in plasma leucine concentrations, suggesting a similar resistance to protein anabolism. Insulin resistance represents a potential mechanism for sarcopenia commonly observed in patients receiving CHD.
authors.affiliation: Division of Nephrology, Vanderbilt University Medical Center, Nashville, Tennessee 37232-2372, USA.
authors.forename: Serpil M
authors.initials: SM
authors.lastname: Deger
authors.forename: Mary B
authors.initials: MB
authors.lastname: Sundell
authors.forename: Edward D
authors.initials: ED
authors.lastname: Siew
authors.forename: Phyllis
authors.initials: P
authors.lastname: Egbert
authors.forename: Charles D
authors.initials: CD
authors.lastname: Ellis
authors.forename: Feng
authors.initials: F
authors.lastname: Sha
authors.forename: T Alp
authors.initials: TA
authors.lastname: Ikizler
authors.forename: Adriana M
authors.initials: AM
authors.lastname: Hung
mesh_terms: D000328:Adult; D001741:Black or African American; D000368:Aged; D000596:Amino Acids / Q000097:blood / Q000493:pharmacokinetics; D001786:Blood Glucose / Q000032:analysis; D001823:Body Composition; D002851:Chromatography, High Pressure Liquid; D003430:Cross-Sectional Studies; D004305:Dose-Response Relationship, Drug; D005260:Female; D015309:Glucose Clamp Technique / Q000379:methods; D006801:Humans; D006946:Hyperinsulinism / Q000097:blood / Q000209:etiology / Q000503:physiopathology; D007328:Insulin / Q000008:administration & dosage / Q000097:blood; D007333:Insulin Resistance; D007930:Leucine / Q000097:blood; D008297:Male; D008875:Middle Aged; D011506:Proteins / Q000378:metabolism*; D006435:Renal Dialysis / Q000009:adverse effects*; D055948:Sarcopenia / Q000209:etiology / Q000503:physiopathology; D012680:Sensitivity and Specificity
chemical_list: D000596:Amino Acids; D001786:Blood Glucose; D007328:Insulin; D011506:Proteins; D007930:Leucine