| A role for the forebrain in mediating time-of-day differences in glucocorticoid counterregulatory responses to hypoglycemia in rats. | |
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MedLine Citation:
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PMID: 17823259 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The time of day influences the magnitude of ACTH and corticosterone responses to hypoglycemia. However, little is known about the mechanisms that impart these time-of-day differences on neuroendocrine CRH neurons in the hypothalamic paraventricular nucleus (PVH). Rats received 0-3 U/kg insulin (or 0.9% saline) to achieve a range of glucose nadir concentrations. Brains were processed to identify phosphorylated ERK1/2 (phospho-ERK1/2)-immunoreactive cells in the PVH and hindbrain and CRH heteronuclear RNA in the PVH. Hypoglycemia did not stimulate ACTH and corticosterone responses in animals unless a glucose concentration of approximately 3.15 mM or below was reached. Critically the glycemic thresholds required to stimulate ACTH and corticosterone release in the morning and night were indistinguishable. Yet glucose concentrations below the estimated glycemic threshold correlated with a greater increase in corticosterone, ACTH, and phospho-ERK1/2-immunoreactive neurons in the PVH at night, compared with morning. In these same animals, the number of phospho-ERK1/2-immunoreactive neurons in the medial part of the nucleus of the solitary tract was unchanged at both times of day. These data collectively support a model whereby changes in forebrain mechanisms alter the sensitivity of neuroendocrine CRH to the hypoglycemia-related information conveyed by ascending catecholaminergic afferents. Circadian clock-driven processes together with glucose-sensing elements in the forebrain would seem to be strong contenders for mediating these effects. |
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Authors:
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Lori M Gorton; Arshad M Khan; Maryann Bohland; Graciela Sanchez-Watts; Casey M Donovan; Alan G Watts |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, N.I.H., Extramural Date: 2007-09-06 |
Journal Detail:
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Title: Endocrinology Volume: 148 ISSN: 0013-7227 ISO Abbreviation: Endocrinology Publication Date: 2007 Dec |
Date Detail:
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Created Date: 2007-11-16 Completed Date: 2008-06-17 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 0375040 Medline TA: Endocrinology Country: United States |
Other Details:
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Languages: eng Pagination: 6026-39 Citation Subset: AIM; IM |
Affiliation:
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The Neuroscience Research Institute, Hedco Neuroscience Building, University of Southern California, Los Angeles, CA 90089-2520, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adrenocorticotropic Hormone
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blood Animals Blood Glucose / metabolism Circadian Rhythm / physiology Corticosterone / blood Glucagon / blood Glucocorticoids / blood Hypoglycemia / blood, physiopathology* Hypoglycemic Agents / administration & dosage* Immunohistochemistry Insulin / administration & dosage*, blood Male Mitogen-Activated Protein Kinase 1 / metabolism Mitogen-Activated Protein Kinase 3 / metabolism Prosencephalon / drug effects*, physiopathology Rats Rats, Sprague-Dawley Time Factors |
| Grant Support | |
ID/Acronym/Agency:
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DK 062471/DK/NIDDK NIH HHS; DK 55257/DK/NIDDK NIH HHS; MH 071108/MH/NIMH NIH HHS; NS 029728/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Blood Glucose; 0/Glucocorticoids; 0/Hypoglycemic Agents; 11061-68-0/Insulin; 50-22-6/Corticosterone; 9002-60-2/Adrenocorticotropic Hormone; 9007-92-5/Glucagon; EC 2.7.11.24/Mitogen-Activated Protein Kinase 1; EC 2.7.11.24/Mitogen-Activated Protein Kinase 3 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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