Record Display for the EPA National Library Catalog


Main Title Central and Sympatho-Adrenal Responses to Insulin in Adult and Neonatal Rats (Journal Version).
Author Lau, C. ; Bartolome, J. V. ; Bartolome, M. B. ; Slotkin, T. A. ;
CORP Author Northrop Services, Inc./Environmental Sciences, Research Triangle Park, NC. ;Duke Univ. Medical Center, Durham, NC. Dept. of Pharmacology.;Health Effects Research Lab., Research Triangle Park, NC.
Publisher c1987
Year Published 1987
Report Number EPA-68-02-4450 ;EPA-68-02-4032; EPA/600/J-87/412;
Stock Number PB89-105589
Additional Subjects Insulin ; Catecholamines ; Adrenal glands ; Central nervous system ; Hypoglycemia ; Laboratory animals ; Secretion ; Newborn animals ; Sympathetic nervous system ; Ornithine decarboxylase ; Aging ; Insulin receptors ; Reprints ; Sympatho-adrenal development
Library Call Number Additional Info Location Last
NTIS  PB89-105589 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 5p
In the mature rat, subcutaneous administration of insulin (0.02 IU/g body wt.) produced hypoglycemia and a profound activation of the sympatho-adrenal pathway, as indicated by a marked depletion of adrenal catecholamines. Cellular glucopenia caused by administration of 2-deoxyglucose also produced a sympatho-adrenal response. In contrast, in 2-day-old rats, the systemic injection of insulin evoked only a small depletion of catecholamines even though severe hypoglycemia was present, and 2-deoxyglucose also produced a diminished response. The central administration of insulin at an equivalent dose (0.02 IU/g brain) stimulated brain ornithine decarboxylase activity in both neonates and adults, but was ineffective in evoking hypoglycemia or adrenal catecholamine release. These results suggest that: (a) direct interaction of insulin with its receptors in the central nervous system is not required for activation of the sympatho-adrenal pathway, and (b) the lack of sensitivity of neonatal adrenal catecholamine release to subcutaneous administration of insulin is likely associated with immaturity of splanchnic neurotransmission rather than with absence of central insulin receptors or impaired peripheral responsiveness to insulin. (Copyright (c) Elsevier Science Publishers B.V.)