Pancreatic beta-cell function in CAPD.
Pancreatic beta-cell function was evaluated in uraemic patients by measuring beta-cell peptides in the peripheral blood after intravenous glucagon (1 mg) stimulation. Patients in chronic renal failure, patients on haemodialysis, and both new and established subjects on continuous ambulatory peritoneal dialysis (CAPD) (10 in each group) were studied and compared to 8 healthy controls. Fasting glucose (3.6-4.4 mmol/l) and insulin concentrations (9.5-11.7 mU/l) were normal and did not differ between the uraemic groups, but c-peptide concentrations were markedly increased in uremia (1.84-2.38 nmol/l) compared to controls (0.48 nmol/l). Following glucagon stimulation an exaggerated blood glucose response with delayed glucose peak was observed, while the peak insulin response to glucagon was normal; however, the return to basal concentrations was delayed in uraemia. The c-peptide response was also exaggerated and peak concentrations in uraemic subjects (3.0-4.3 nmol/l) were significantly greater than controls (1.5 nmol/l). The response of CAPD patients was similar to those on haemodialysis and non-dialysed uraemic patients. The abnormalities seen were due to uraemia, and CAPD treatment had no specific adverse effect on beta-cell function. Thus, from this data there was no evidence that CAPD per se is detrimental to beta-cell integrity.
D002096:C-Peptide / Q000032:analysis; D003429:Cross Reactions; D005934:Glucagon / Q000494:pharmacology; D006801:Humans; D007328:Insulin / Q000097:blood; D007515:Islets of Langerhans / Q000503:physiopathology*; D010531:Peritoneal Dialysis, Continuous Ambulatory; D011384:Proinsulin / Q000276:immunology; D014511:Uremia / Q000503:physiopathology*
D002096:C-Peptide; D007328:Insulin; D005934:Glucagon; D011384:Proinsulin