title: Influence of hemodialysis on incretin hormones and insulin secretion in diabetic and non-diabetic patients.
abstract: BACKGROUND
  Incretin hormones are secreted in the gut after a meal and stimulate insulin production. Both major incretins, that is, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), are eliminated by the kidneys. Little is known about the influence of end-stage renal disease (ESRD) on the incretin axis. The aim of the study was to assess the effect of the commencement of chronic hemodialysis (HD) therapy on serum GLP-1 and GIP, and insulin sensitivity in diabetic and non-diabetic patients.
  
  
  METHODS
  The study comprised 56 patients (23 F, 33 M; mean age 57 ± 14 years) with ESRD in the course of diabetic nephropathy (n = 23) and non-diabetic renal diseases (n = 34) who started chronic HD. Glucose metabolism, including incretin hormones concentration, was assessed before the first HD session and repeated after the first 6 months of the therapy.
  
  
  RESULTS
  After 6 months of HD, a significant increase in fasting GLP-1 concentration was observed in both diabetic and non-diabetic patients [by 2.27 pmol/l (45 %) and 1.28 pmol/l (22 %), respectively, p = 0.0003]. Serum GIP increased significantly only in diabetic patients [by 30.9 pg/ml (55 %); p = 0.008]. No significant change of fasting glucose was found but HOMA-IR and serum insulin decreased significantly in diabetic patients (p = 0.01 and p = 0.008, respectively). In contrast, HOMA-B was unchanged in both groups. Changes of HOMA-IR did not significantly correlate with serum GLP-1 or GIP concentrations.
  
  
  CONCLUSIONS
  Our results indicate that starting the hemodialysis therapy helps to restore the incretin axis in particular in patients with the diabetic kidney disease.
authors.affiliation: Department of Nephrology, Hypertension and Kidney Transplantation, Medical University of Lodz, Kopcińskiego 22, 90153, Lodz, Poland, ania_pl@wp.pl.
authors.forename: Anna
authors.initials: A
authors.lastname: Masajtis-Zagajewska
authors.forename: Ilona
authors.initials: I
authors.lastname: Kurnatowska
authors.forename: Małgorzata
authors.initials: M
authors.lastname: Wajdlich
authors.forename: Marta
authors.initials: M
authors.lastname: Jagodzińska
authors.forename: Michał
authors.initials: M
authors.lastname: Nowicki
mesh_terms: D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000378:metabolism; D016022:Case-Control Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood; D003928:Diabetic Nephropathies / Q000097:blood* / Q000503:physiopathology; D005215:Fasting; D005260:Female; D005749:Gastric Inhibitory Polypeptide / Q000097:blood*; D052216:Glucagon-Like Peptide 1 / Q000097:blood*; D006706:Homeostasis; D006801:Humans; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D007333:Insulin Resistance; D000078790:Insulin Secretion; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis; D013997:Time Factors
chemical_list: D001786:Blood Glucose; D007328:Insulin; D005749:Gastric Inhibitory Polypeptide; D052216:Glucagon-Like Peptide 1