6
Views
0
CrossRef citations to date
0
Altmetric
Original Article

Metabolic effect of islet B-cell function in insulin-treated diabetes

, , &
Pages 337-343 | Received 21 Jul 1988, Accepted 26 Nov 1988, Published online: 08 Jul 2009
 

Abstract

We studied the relationship between endogenous insulin secretion and fasting levels of plasma free fatty acids (FFA), plasma acetoacetate plus plasma 3-hydroxybutyrate (total ketone bodies), blood glucose, and HbAl in 132 diabetic outpatients treated with conventional insulin regimens. Patients were divided into four groups according to plasma C-peptide concentration after intravenous stimulation with glucagon: one group with C-peptide stimulation <0.06 nmol/1, one group with C-peptide stimulation 0.06<0.32 nmol/1, one group with C-peptide stimulation 0.32-<0.60 nmol/1, and one group with C-peptide stimulation 0.60 nmol/1. According to clinical criteria the prevalence of insulin-dependent diabetes mellitus was approximately 90% in patients with C-peptide stimulation <0.32 nmol/1, approximately 25% in patients with C-peptide stimulation from 0.32-<0.60 nmol/1, and approximately 10% in patients with C-peptide stimulation ×0.60 nmol/1. All metabolic variables were significantly higher in patients without detectable C-peptide in plasma when compared to values found in patients with C-peptide stimulation from 0.06-<0.32 nmol/1. These two patient groups also had similar peripheral plasma free insulin levels and were comparable according to age, sex, and body mass index. In a subgroup of 25 patients with C-peptide stimulation <0.06 nmol/1 matched according to sex and HbAl value with 25 patients with C-peptide stimulation from 0.06-<0.32 nmol/1 the higher values of FFA and fasting blood glucose were still found among patients of the former group. In conclusion, preserved C-peptide secretion protects against elevations in overnight fasting values of FFA, ketone bodies, and blood glucose in insulin treated diabetic outpatients. The protection effect against ketogenesis and hyperglycaemia may, in part, be due to a direct effect of portal insulin on the liver.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.