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Gastrointestinal factors contribute to glucometabolic disturbances in nondiabetic patients with end-stage renal disease

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Authors:
  • Idorn, Thomas ;
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    Department of Clinical Medicine, Faculty of Health and Medical Sciences, Københavns Universitet
  • Knop, Filip K ;
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    Department of Clinical Medicine, Department of Clinical Medicine, Faculty of Health and Medical Sciences, Københavns Universitet
  • Jørgensen, Morten ;
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    Rigshospitalet
  • Holst, Jens Juul ;
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    Orcid logo0000-0001-6853-3805
    Endocrinology and Metabolism, Department of Biomedical Sciences, Faculty of Health and Medical Sciences, Københavns Universitet
  • Hornum, Mads ;
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    Department of Clinical Medicine, Department of Clinical Medicine, Faculty of Health and Medical Sciences, Københavns Universitet
  • Feldt-Rasmussen, Bo
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    Section of Surgery and Internal Medicine, Department of Clinical Medicine, Faculty of Health and Medical Sciences, Københavns Universitet
DOI:
10.1038/ki.2012.460
Abstract:
Nondiabetic patients with end-stage renal disease (ESRD) have disturbed glucose metabolism, the underlying pathophysiology of which is unclear. To help elucidate this, we studied patients with ESRD and either normal or impaired glucose tolerance (10 each NGT or IGT, respectively) and 11 controls using an oral glucose tolerance test and an isoglycemic intravenous glucose infusion on separate days. Plasma glucose, insulin, glucagon, and incretin hormones were measured repeatedly, and gastrointestinal-mediated glucose disposal (GIGD) based on glucose amounts utilized, and incretin effect based on incremental insulin responses, were calculated. The GIGD was significantly reduced in both ESRD groups compared with controls. Incretin effects were 69% (controls), 55% (ESRD with NGT), and 41% (ESRD with IGT), with a significant difference between controls and ESRDs with IGT. Fasting concentrations of glucagon and incretin hormones were significantly increased in patients with ESRD. Glucagon suppression was significantly impaired in both groups with ESRD compared with controls, while the baseline-corrected incretin hormone responses were unaltered between groups. Thus, patients with ESRD had reduced GIGD, a diminished incretin effect in those with IGT, and severe fasting hyperglucagonemia that seemed irrepressible in response to glucose stimuli. These factors may contribute to disturbed glucose metabolism in ESRD.
Type:
Journal article
Language:
English
Published in:
Kidney International, 2013, Vol 83, Issue 5, p. 915-23
Keywords:
Journal Article; Research Support, Non-U.S. Gov't; Adult; Analysis of Variance; Area Under Curve; Biological Markers; Blood Glucose; Case-Control Studies; Fasting; Female; Gastric Inhibitory Polypeptide; Gastrointestinal Tract; Glucagon; Glucagon-Like Peptide 1; Glucose Metabolism Disorders; Glucose Tolerance Test; Humans; Incretins; Insulin; Kidney Failure, Chronic; Linear Models; Male; Middle Aged; Time Factors
Main Research Area:
Medical science
Publication Status:
Published
Review type:
Peer Review
Submission year:
2013
Scientific Level:
Scientific
ID:
241136779

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