Source:http://linkedlifedata.com/resource/pubmed/id/18182467
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2008-3-7
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pubmed:abstractText |
Antecedent increases of corticosteroids can blunt counterregulatory responses to subsequent stress. Our aim was to determine whether prior activation of type I corticosteroid (mineralocorticoid) or type II corticosteroid (glucocorticoid) receptors blunts counterregulatory responses to subsequent hypoglycemia. Healthy volunteers participated in five randomized 2-day protocols. Day 1 involved morning and afternoon 2-h hyperinsulinemic (9 pmol.kg(-1).min(-1)) euglycemic clamps (PE; n = 14), hypoglycemic clamps (PH; n = 14), or euglycemic clamps with oral fludrocortisone (PE + F; type I agonist, 0.2 mg, n = 14), oral dexamethasone (PE + D; type II agonist, 0.75 mg, n = 13), or both (PE + F + D; n = 14). Day 2 was identical in all protocols and consisted of a 2-h hyperinsulinemic hypoglycemic clamp. Day 2 insulin (625 +/- 40 pmol/l) and glucose (2.9 +/- 0.1 mmol/l) levels were similar among groups. Levels of epinephrine, norepinephrine, glucagon, growth hormone, and MSNA were significantly blunted by prior activation of both type I and type II corticosteroid receptors to PE. Prior activation of both corticosteroid receptors also significantly blunted NEFA during subsequent hypoglycemia. Thus, levels of a wide spectrum of key counterregulatory mechanisms (neuroendocrine, ANS, and metabolic) were blunted by antecedent pharmacological stimulation of either type I or type II corticosteroid receptors in healthy man. These data suggest that activation of type I corticosteroid receptors in man can have acute and profound regulating effects on physiological stress in man. Both type I and type II corticosteroid receptors may be involved in the multiple mechanisms controlling counterregulatory responses to hypoglycemia in healthy man.
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pubmed:grant |
http://linkedlifedata.com/resource/pubmed/grant/1-RO1-DK-69803,
http://linkedlifedata.com/resource/pubmed/grant/K23 RR020783-02,
http://linkedlifedata.com/resource/pubmed/grant/MO1-RR-00095,
http://linkedlifedata.com/resource/pubmed/grant/P01-HL-056693-DK,
http://linkedlifedata.com/resource/pubmed/grant/P60-DK-20593
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Blood Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Dexamethasone,
http://linkedlifedata.com/resource/pubmed/chemical/Fatty Acids, Nonesterified,
http://linkedlifedata.com/resource/pubmed/chemical/Fludrocortisone,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Glucocorticoid,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Mineralocorticoid
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0193-1849
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
294
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
E506-12
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pubmed:dateRevised |
2010-6-25
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pubmed:meshHeading |
pubmed-meshheading:18182467-Adult,
pubmed-meshheading:18182467-Blood Glucose,
pubmed-meshheading:18182467-Dexamethasone,
pubmed-meshheading:18182467-Fatty Acids, Nonesterified,
pubmed-meshheading:18182467-Female,
pubmed-meshheading:18182467-Fludrocortisone,
pubmed-meshheading:18182467-Glucose Clamp Technique,
pubmed-meshheading:18182467-Homeostasis,
pubmed-meshheading:18182467-Humans,
pubmed-meshheading:18182467-Hyperinsulinism,
pubmed-meshheading:18182467-Hypoglycemia,
pubmed-meshheading:18182467-Male,
pubmed-meshheading:18182467-Receptors, Glucocorticoid,
pubmed-meshheading:18182467-Receptors, Mineralocorticoid
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pubmed:year |
2008
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pubmed:articleTitle |
Stimulation of both type I and type II corticosteroid receptors blunts counterregulatory responses to subsequent hypoglycemia in healthy man.
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pubmed:affiliation |
Department of Medicine, Div. of Diabetes, Endocrinology, and Metabolism,Vanderbilt University Medical Center 7465 MRB IV, Nashville, TN 37232-0475, USA.
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pubmed:publicationType |
Journal Article,
Randomized Controlled Trial,
Research Support, N.I.H., Extramural
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