Publication Date:
1979-06-08
Description:
The reduction of glycolysis by hypoglycemia or the glucose analog 2-deoxy-D-glucose (2DG) stimulates compensatory sympathetic alterations of metabolism. Considerable attention has been focused on the hypothalamus as the probable locus of requisite metabolic signal detection. We report, however, that unanesthetized chronically decerebrate rats are capable of exhibiting sympathoadrenal hyperglycemia in response to the metabolic challenge presented by 2DG. This findings demonstrates that the forebrain is not necessary for glucoprivic stimulation of this reflex. Since cervical cord transection has been shown to eliminate hyperglycemia induced by 2DG, we conclude that the caudal brainstem contains an essential part of the neural mechanism which both detects metabolic need and ameliorates that need through the release of stored fuels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉DiRocco, R J -- Grill, H J -- New York, N.Y. -- Science. 1979 Jun 8;204(4397):1112-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/451558" target="_blank"〉PubMed〈/a〉
Keywords:
Adrenal Glands/physiology
;
Afferent Pathways
;
Animals
;
Blood Glucose/*metabolism
;
Brain Stem/*physiology
;
Decerebrate State
;
Deoxy Sugars/*pharmacology
;
Deoxyglucose/*pharmacology
;
*Energy Metabolism
;
Hypothalamus/*physiology
;
Rats
;
Reflex/physiology
;
Sympathetic Nervous System/physiology
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
