| Effects of differing antecedent increases of plasma cortisol on counterregulatory responses during subsequent exercise in type 1 diabetes. | |
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MedLine Citation:
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PMID: 19509020 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: Antecedent hypoglycemia can blunt neuroendocrine and autonomic nervous system responses to next-day exercise in type 1 diabetes. The aim of this study was to determine whether antecedent increase of plasma cortisol is a mechanism responsible for this finding. RESEARCH DESIGN AND METHODS: For this study, 22 type 1 diabetic subjects (11 men and 11 women, age 27 +/- 2 years, BMI 24 +/- 1 kg/m(2), A1C 7.9 +/- 0.2%) underwent four separate randomized 2-day protocols, with overnight normalization of blood glucose. Day 1 consisted of morning and afternoon 2-h hyperinsulinemic- (9 pmol x kg(-1) x min(-1)) euglycemic clamps (5.1 mmol/l), hypoglycemic clamps (2.9 mmol/l), or euglycemic clamps with a physiologic low-dose intravenous infusion of cortisol to reproduce levels found during hypoglycemia or a high-dose infusion, which resulted in further twofold greater elevations of plasma cortisol. Day 2 consisted of 90-min euglycemic cycling exercise at 50% Vo(2max). RESULTS: During exercise, glucose levels were equivalently clamped at 5.1 +/- 0.1 mmol/l and insulin was allowed to fall to similar levels. Glucagon, growth hormone, epinephrine, norepinephrine, and pancreatic polypeptide responses during day 2 exercise were significantly blunted following antecedent hypoglycemia, low- and high-dose cortisol, compared with antecedent euglycemia. Endogenous glucose production and lipolysis were also significantly reduced following day 1 low- and high-dose cortisol. CONCLUSIONS: Antecedent physiologic increases in cortisol (equivalent to levels occurring during hypoglycemia) resulted in blunted neuroendocrine, autonomic nervous system, and metabolic counterregulatory responses during subsequent exercise in subjects with type 1 diabetes. These data suggest that prior elevations of cortisol may play a role in the development of exercise-related counterregulatory failure in those with type 1 diabetes. |
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Authors:
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Shichun Bao; Vanessa J Briscoe; Donna B Tate; Stephen N Davis |
Publication Detail:
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Type: Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural Date: 2009-06-09 |
Journal Detail:
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Title: Diabetes Volume: 58 ISSN: 1939-327X ISO Abbreviation: Diabetes Publication Date: 2009 Sep |
Date Detail:
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Created Date: 2009-09-01 Completed Date: 2009-09-30 Revised Date: 2010-09-02 |
Medline Journal Info:
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Nlm Unique ID: 0372763 Medline TA: Diabetes Country: United States |
Other Details:
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Languages: eng Pagination: 2100-8 Citation Subset: AIM; IM |
Affiliation:
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Department of Medicine, Division of Diabetes, Endocrinology, and Metabolism, Vanderbilt University Medical Center, Nashville, Tennessee, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adult Autonomic Nervous System / physiology* Blood Glucose / metabolism Diabetes Mellitus, Type 1 / blood, physiopathology* Epinephrine / blood Exercise / physiology* Female Glucose Clamp Technique Humans Hydrocortisone / administration & dosage*, blood* Hyperinsulinism / blood, physiopathology Hypoglycemia / blood, physiopathology* Infusions, Intravenous Insulin / blood Male |
| Grant Support | |
ID/Acronym/Agency:
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DK069803/DK/NIDDK NIH HHS; DK20593/DK/NIDDK NIH HHS; HL056693/HL/NHLBI NIH HHS; RR00095/RR/NCRR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Blood Glucose; 11061-68-0/Insulin; 50-23-7/Hydrocortisone; 51-43-4/Epinephrine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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