Journal article
Dehydroepiandrosterone sulfate and β-cell function: Enhanced glucose-induced insulin secretion and altered gene expression in rodent pancreatic β-cells
Diabetes (New York, N.Y.), Vol.49(12), pp.2012-2020
2000
DOI: 10.2337/diabetes.49.12.2012
PMID: 11118002
Abstract
Administration of dehydroepiandrosterone (DHEA), or its sulfated form (DHEAS), controls hyperglycemia in diabetic rodents without directly altering insulin sensitivity. We show that DHEAS enhanced glucose-stimulated insulin secretion when administered in vivo to rats or in vitro to beta-cell lines, without changing cellular insulin content. Insulin secretion increased from 3 days of steroid exposure in vitro, suggesting that DHEAS did not directly activate the secretory processes. DHEAS selectively increased the beta-cell mRNA expression of acyl CoA synthetase-2 and peroxisomal acyl CoA oxidase in a time-dependent manner. Although DHEAS is a peroxisomal proliferator, it did not alter the mRNA expression of peroxisomal proliferator-activated receptor (PPAR) alpha or beta, or enhance the activity of transfected PPAR alpha, beta, or gamma in vitro. Thus, DHEAS directly affected the beta-cell to enhance glucose-stimulated insulin secretion and increased the mRNA expression of specific beta-cell mitochondrial and peroxisomal lipid metabolic enzymes. This effect of DHEAS on insulin secretion may contribute to the amelioration of hyperglycemia seen in various rodent models of diabetes.
Details
- Title: Subtitle
- Dehydroepiandrosterone sulfate and β-cell function: Enhanced glucose-induced insulin secretion and altered gene expression in rodent pancreatic β-cells
- Creators
- Joseph S DILLON - Division of Endocrinology, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa, United StatesGordon C YANEY - Diabetes and Metabolism Unit, Evans Department of Medicine, Boston Medical Center, Boston, Massachusetts, United StatesDavid J WAXMAN - Department of Biology, Boston University, Boston, Massachusetts, United StatesBarbara E CORKEY - Diabetes and Metabolism Unit, Evans Department of Medicine, Boston Medical Center, Boston, Massachusetts, United StatesYUANCHUN ZHOU - Department of Biology, Boston University, Boston, Massachusetts, United StatesNicolas VOILLEY - Department of Nutrition, University of Montreal and the CHUM, Campus Notre Dame, Centre de Recherche L.-C. Simard, Montreal, Quebec, CanadaSusan BOWEN - Division of Endocrinology, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa, United StatesStuart CHIPKIN - Diabetes and Metabolism Unit, Evans Department of Medicine, Boston Medical Center, Boston, Massachusetts, United StatesCheryl R BLISS - Diabetes and Metabolism Unit, Evans Department of Medicine, Boston Medical Center, Boston, Massachusetts, United StatesVera SCHULTZ - Diabetes and Metabolism Unit, Evans Department of Medicine, Boston Medical Center, Boston, Massachusetts, United StatesFrans C SCHUIT - Department of Biochemistry, Diabetes Research Center, Vrije Universiteit Brussel, Laarbeeklaan 103, Brussels, BelgiumMarc PRENTKI - Department of Nutrition, University of Montreal and the CHUM, Campus Notre Dame, Centre de Recherche L.-C. Simard, Montreal, Quebec, Canada
- Resource Type
- Journal article
- Publication Details
- Diabetes (New York, N.Y.), Vol.49(12), pp.2012-2020
- Publisher
- American Diabetes Association
- DOI
- 10.2337/diabetes.49.12.2012
- PMID
- 11118002
- ISSN
- 0012-1797
- eISSN
- 1939-327X
- Language
- English
- Date published
- 2000
- Academic Unit
- Fraternal Order of Eagles Diabetes Research Center; Endocrinology and Metabolism; Internal Medicine
- Record Identifier
- 9984094766102771
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