Effects of Intravenous Glucose Load on Insulin Secretion in Patients With Ketosis-Prone Diabetes During Near-Normoglycemia Remission

• Type of Material: Article
• Authors: Aidar R. Gosmanov, Emory University; Dawn Smiley, Emory University; Gonzalo Robalino, Emory University; Joselita M. Siqueira, Emory University; Limin Peng, Emory University; Abbas E. Kitabchi, University of Tennessee; Guillermo Umpierrez, Emory University
• Language: English
• Date: 2010-01-12
• Publisher: American Diabetes Association
• Publication Version: Final Published Version
• Copyright Statement: © 2010 by the American Diabetes Association
• License: Creative Commons Attribution-NonCommerical-NoDerivs 3.0 Unported
• Final Published Version (URL): http://care.diabetesjournals.org/content/33/4/854
• Title of Journal or Parent Work: Diabetes Care
• ISSN: 0149-5992
• Volume: 33
• Issue: 4
• Start Page: 854
• End Page: 860
• Grant/Funding Information: This study was supported by research grants from the American Diabetes Association (grant 7-03-CR-35) and the National Institutes of Health (grants R03-DK-073190-01 and M01-RR00039).
• Research Categories: Health Sciences, Public Health; Health Sciences, Medicine and Surgery

Abstract

OBJECTIVE Most patients with ketosis-prone type 2 diabetes (KPD) discontinue insulin therapy and remain in near-normoglycemic remission. The aim of this study was to determine the effect of glucotoxicity on β-cell function during remission in obese patients with KPD. RESEARCH DESIGN AND METHODS Age- and BMI-matched obese African Americans with a history of KPD (n = 8), severe hyperglycemia but without ketosis (ketosis-resistant type 2 diabetes, n = 7), and obese control subjects (n = 13) underwent intravenous infusion of 10% dextrose at a rate of 200 mg per m2/min for 20 h. β-Cell function was assessed by changes in insulin and C-peptide concentrations during dextrose infusion and by changes in acute insulin response (AIR) and first-phase insulin release (FPIR) to arginine stimulation before and after dextrose infusion. RESULTS The mean ± SD time to discontinue insulin therapy was 7.1 ± 1.7 weeks in KPD and 9.6 ± 2.3 weeks in ketosis-resistant type 2 diabetes (NS). During a 20-h dextrose infusion, changes in insulin, C-peptide, and the C-peptide–to–glucose ratio were similar among diabetic and control groups. During dextrose infusion, subjects with ketosis-resistant type 2 diabetes had greater areas under the curve for blood glucose than subjects with KPD and control subjects (P < 0.05). The AIR and FPIR to arginine stimulation as well as glucose potentiation to arginine assessed before and after dextrose infusion were not different among the study groups. CONCLUSIONS Near-normoglycemia remission in obese African American patients with KPD and ketosis-resistant type 2 diabetes is associated with a remarkable recovery in basal and stimulated insulin secretion. At near-normoglycemia remission, patients with KPD displayed a pattern of insulin secretion similar to that of patients with ketosis-resistant type 2 diabetes and obese nondiabetic subjects.