Postprandial responses of incretin and pancreatic hormones in non-diabetic patients with end-stage renal disease
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Postprandial responses of incretin and pancreatic hormones in non-diabetic patients with end-stage renal disease. / Idorn, Thomas; Knop, Filip K; Jørgensen, Morten; Holst, Jens Juul; Hornum, Mads; Feldt-Rasmussen, Bo.
In: Nephrology, Dialysis, Transplantation, Vol. 29, No. 1, 01.2014, p. 119-27.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Postprandial responses of incretin and pancreatic hormones in non-diabetic patients with end-stage renal disease
AU - Idorn, Thomas
AU - Knop, Filip K
AU - Jørgensen, Morten
AU - Holst, Jens Juul
AU - Hornum, Mads
AU - Feldt-Rasmussen, Bo
PY - 2014/1
Y1 - 2014/1
N2 - BACKGROUND: Patients with end-stage renal disease (ESRD) have glucometabolic disturbances resulting in a high prevalence of prediabetes. The underlying pathophysiology remains unclear, but may prove important for the strategies employed to prevent progression to overt diabetes. Meal-induced release of the insulinotropic gut-derived incretin hormones and pancreatic hormones play a critical role in the maintenance of a normal postprandial glucose tolerance.METHODS: We studied patients with ESRD and either normal (n = 10) or impaired (n = 10) glucose tolerance, and control subjects (n = 11). Plasma concentrations of glucose, insulin, glucagon, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and paracetamol were measured repeatedly during a standardized 4-h liquid meal including 1.5 g paracetamol (added for evaluation of gastric emptying).RESULTS: Fasting glucose and postprandial glucose responses were comparable between groups (P > 0.082). Patients with ESRD exhibited higher fasting levels of GIP and glucagon compared with controls (P < 0.001). Baseline-corrected GLP-1 and glucagon responses were enhanced (P < 0.002), baseline-corrected insulin responses and insulin excursions were reduced (P < 0.035), and paracetamol excursions were delayed (P < 0.024) in patients with ESRD compared with controls. None of the variables differed between the two ESRD subgroups.CONCLUSIONS: Non-diabetic patients with ESRD were characterized by reduced postprandial insulin responses despite increased secretion of the insulinotropic incretin hormone GLP-1. Fasting levels and baseline-corrected responses of glucagon were elevated and gastric emptying was delayed in the ESRD patients. These perturbations seem to be caused by uraemia per se and may contribute to the disturbed glucose metabolism in ESRD patients.
AB - BACKGROUND: Patients with end-stage renal disease (ESRD) have glucometabolic disturbances resulting in a high prevalence of prediabetes. The underlying pathophysiology remains unclear, but may prove important for the strategies employed to prevent progression to overt diabetes. Meal-induced release of the insulinotropic gut-derived incretin hormones and pancreatic hormones play a critical role in the maintenance of a normal postprandial glucose tolerance.METHODS: We studied patients with ESRD and either normal (n = 10) or impaired (n = 10) glucose tolerance, and control subjects (n = 11). Plasma concentrations of glucose, insulin, glucagon, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and paracetamol were measured repeatedly during a standardized 4-h liquid meal including 1.5 g paracetamol (added for evaluation of gastric emptying).RESULTS: Fasting glucose and postprandial glucose responses were comparable between groups (P > 0.082). Patients with ESRD exhibited higher fasting levels of GIP and glucagon compared with controls (P < 0.001). Baseline-corrected GLP-1 and glucagon responses were enhanced (P < 0.002), baseline-corrected insulin responses and insulin excursions were reduced (P < 0.035), and paracetamol excursions were delayed (P < 0.024) in patients with ESRD compared with controls. None of the variables differed between the two ESRD subgroups.CONCLUSIONS: Non-diabetic patients with ESRD were characterized by reduced postprandial insulin responses despite increased secretion of the insulinotropic incretin hormone GLP-1. Fasting levels and baseline-corrected responses of glucagon were elevated and gastric emptying was delayed in the ESRD patients. These perturbations seem to be caused by uraemia per se and may contribute to the disturbed glucose metabolism in ESRD patients.
U2 - 10.1093/ndt/gft353
DO - 10.1093/ndt/gft353
M3 - Journal article
C2 - 24078334
VL - 29
SP - 119
EP - 127
JO - Nephrology, Dialysis, Transplantation
JF - Nephrology, Dialysis, Transplantation
SN - 0931-0509
IS - 1
ER -
ID: 117853306