Document Detail


Investigation of the mechanisms contributing to the compensatory increase in insulin secretion during dexamethasone-induced insulin resistance in rhesus macaques.
MedLine Citation:
PMID:  23151361     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Dexamethasone has well-described effects to induce insulin resistance and increase insulin secretion. Herein, we examined potential contributors to the effect of dexamethasone to increase insulin secretion in rhesus macaques. Six male rhesus macaques received daily injections of either saline or dexamethasone (0.25 mg/kg i.m. for 7 days) in random order with 3 weeks between treatments. At the end of the treatment period, animals were fasted overnight and underwent a feeding study the next day, during which blood samples were taken before and for 60 min after a meal in order to assess islet hormone and incretin secretion. Dexamethasone induced marked increases in fasting plasma insulin, glucagon, leptin, and adiponectin concentrations (P<0.05). Surprisingly, the glycemic response after meal ingestion was decreased twofold during dexamethasone treatment (P<0.05). Dexamethasone-treated animals exhibited a significant increase in both insulin and glucose-dependent insulinotropic polypeptide (GIP) secretion during the feeding study (P<0.05). However, glucagon-like peptide-1 secretion was significantly lower in dexamethasone-treated animals compared with controls (P<0.01). Fasting and meal-stimulated pancreatic polypeptide concentrations (an index of the parasympathetic input to the islet) did not differ between saline and dexamethasone treatments. However, the proinsulin:insulin ratio was decreased throughout the feeding study with dexamethasone treatment suggesting an improvement of β-cell function (P<0.05). In conclusion, the maintenance of euglycemia and reduction of postprandial glycemia with short-term dexamethasone treatment appears to be due to the marked elevations of fasting and meal-stimulated insulin secretion. Furthermore, increases in postprandial GIP secretion with dexamethasone treatment appear to contribute to the effect of dexamethasone treatment to increase insulin secretion.
Authors:
Bethany P Cummings; Andrew A Bremer; Timothy J Kieffer; David D'Alessio; Peter J Havel
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2013-01-18
Journal Detail:
Title:  The Journal of endocrinology     Volume:  216     ISSN:  1479-6805     ISO Abbreviation:  J. Endocrinol.     Publication Date:  2013 Feb 
Date Detail:
Created Date:  2013-01-21     Completed Date:  2013-03-11     Revised Date:  2013-05-31    
Medline Journal Info:
Nlm Unique ID:  0375363     Medline TA:  J Endocrinol     Country:  England    
Other Details:
Languages:  eng     Pagination:  207-15     Citation Subset:  IM    
Affiliation:
Department of Molecular Biosciences, School of Veterinary Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA. bpcummings@ucdavis.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Glucose / metabolism
Dexamethasone / pharmacology*
Fasting / blood
Insulin / secretion*
Insulin Resistance / physiology*
Macaca mulatta
Male
Postprandial Period / drug effects
Receptors, Gastrointestinal Hormone / metabolism
Grant Support
ID/Acronym/Agency:
1RC1DK087307-01/DK/NIDDK NIH HHS; AT-002993/AT/NCCAM NIH HHS; AT-003545/AT/NCCAM NIH HHS; DK-095980/DK/NIDDK NIH HHS; HL-075675/HL/NHLBI NIH HHS; HL-091333/HL/NHLBI NIH HHS; HL-107256/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Insulin; 0/Receptors, Gastrointestinal Hormone; 0/gastric inhibitory polypeptide receptor; 50-02-2/Dexamethasone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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