Induction of β-Cell Rest in Type 1 Diabetes: Studies on the effects of octreotide and diazoxide
- Elisabeth Björk, MD, PHD,
- Christian Berne, MD, PHD and
- F Anders Karlsson, MD, PHD
- Address correspondence and reprint requests to Anders Karlsson, Section of Endocrinology and Diabetes, Department of Medicine, University Hospital, S-751 85 Uppsala, Sweden. E-mail: anders.karlsson{at}medicin.uu.se
Abstract
OBJECTIVE To evaluate the inhibitory effects of octreotide and diazoxide on insulin secretion in patients with type 1 diabetes and measurable levels of circulating C-peptide.
RESEARCH DESIGN AND METHODS Diazoxide was given to six patients during a 7-day period (100 mg three times daily), followed by a 3-week washout. Subsequently, octreotide (50 micrograms, three times daily) was administered subcutaneously for 7 days. Pre- and post- prandial blood glucose and serum C-peptide concentrations were measured before medication (control) and on day 7 of each medication period. Glucagon-stimulated C-peptide was determined in the morning before medication and on the day after each treatment period.
RESULTS Diazoxide inhibited glucagon-stimulated C-peptide secretion (mean increment 0.08 nmol/l vs. 0.18 nmol/l, P < 0.05), whereas octreotide had no such effect. Both reduced the pre- and postprandial serum C-peptide concentrations (P < 0.05), octreotide being the more potent in this respect. A reduction in basal and meal-related blood glucose was observed during octreotide treatment, whereas the glucose concentrations tended to be higher during treatment with diazoxide than during the 24-h control period.
CONCLUSIONS The study indicates that the two drugs reduce insulin output by different mechanisms. Diazoxide inhibits hormonal release directly on the beta-cells, whereas octreotide exerts its effect indirectly, presumably by multiple actions on insulin sensitivity and insulin-releasing hormones. The results suggest that each drug is capable of inducing beta-cell rest in type 1 diabetes.
- Received July 18, 1997.
- Accepted November 12, 1997.
- Copyright © 1998 by the American Diabetes Association











