Dysfunctional pancreatic β-cells of critical stress play a more prominent role in the development of stress diabetes in critically burned Korean subjects

The purposes of this study are to identify the predictive parameters for the development of stress-induced hyperglycemia and to investigate the glucose metabolic homeostasis in critically burned Korean subjects. We conducted a prospective cross-sectional study of adult patients with glucose manageme...

Full description

Saved in:
Bibliographic Details
Published inMetabolism, clinical and experimental Vol. 59; no. 9; pp. 1307 - 1315
Main Authors Byung-Wan, Lee, Jun, Hur, Yim, Hae-Jun, Park, Jae-Bong, Woo, Heungjeong, Yoo, Hyung-Joon
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.09.2010
Subjects
Online AccessGet full text
ISSN0026-0495
1532-8600
1532-8600
DOI10.1016/j.metabol.2009.11.022

Cover

More Information
Summary:The purposes of this study are to identify the predictive parameters for the development of stress-induced hyperglycemia and to investigate the glucose metabolic homeostasis in critically burned Korean subjects. We conducted a prospective cross-sectional study of adult patients with glucose management targeting fasting and postprandial blood glucose levels less than 140 and 200 mg/dL, respectively, in patients with unrecognized diabetes. Clinical and laboratory stress parameters and insulin secretory and sensitivity parameters were assessed. Stimulated C-peptide and 24-hour urinary free cortisol predicted new-onset stress diabetes requiring insulin therapy. The subjects requiring insulin therapy were leaner and more insulin sensitive than insulin-free subjects, without significance. Glycated hemoglobin, stimulated C-peptide, homeostasis model assessment of insulin resistance, and age had a significant influence on the mean daily dose of insulin. Our present data showed that Korean subjects with dysfunctional pancreatic β-cells of critical stress are prone to become stress diabetic and require more insulin to control the hyperglycemia.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0026-0495
1532-8600
1532-8600
DOI:10.1016/j.metabol.2009.11.022