File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Effects of recurrent hyperinsulinemia with and without hypoglycemia on counterregulation in diabetic rats

TitleEffects of recurrent hyperinsulinemia with and without hypoglycemia on counterregulation in diabetic rats
Authors
KeywordsGlucose production
Insulin sensitivity
Hypoglycemic glucose clamp
Epinephrine
Issue Date2002
Citation
American Journal of Physiology - Endocrinology and Metabolism, 2002, v. 282, n. 6 45-6, p. E1369-E1379 How to Cite?
AbstractTo understand the mechanisms whereby recurrent hypoglycemia increases the risk of subsequent hypoglycemia, it was necessary to differentiate the effects of recurrent hyperinsulinemia from those of hyperinsulinemic hypoglycemia. We examined basal and hypoglycemic endocrine function in normal rats, streptozotocin-diabetic controls, and diabetic rats exposed to 4 days of 2 episodes/day of hyperinsulinemic hypoglycemia (DH) or hyperinsulinemic hyperglycemia (DI). DH and DI rats differentiated the effects of hyperinsulinemia from those of hypoglycemia. In diabetic controls, basal plasma ACTH tended to be increased, and plasma corticosterone, plasma somatostatin, and pancreatic prosomatostatin and proglucagon mRNA were increased (P < 0.05) vs. normal rats. These parameters were normalized in DH and DI rats. In diabetic controls, glucagon, epinephrine, norepinephrine, corticosterone, and peak glucose production responses to hypoglycemia were reduced (P < 0.05) vs. normal rats. In DI rats, epinephrine responses were normalized. Conversely, DH rats displayed marked further impairment of epinephrine and glucose production responses and increased peripheral insulin sensitivity (P < 0.05 vs. diabetic controls). Both insulin regimens partially normalized glucagon and fully normalized norepinephrine and corticosterone responses. In summary, recurrent hyperinsulinemia in diabetic rats normalized most pituitary-adrenal, sympathoadrenal, and pancreatic parameters. However, concurrent hypoglycemia further impaired epinephrine and glucose production responses and increased insulin sensitivity. We conclude that 1) recurrent hypoglycemia may increase the risk of subsequent hypoglycemia by increasing insulin sensitivity, and 2) epinephrine counterregulation is particularly sensitive to impairment by recurrent hypoglycemia.
Persistent Identifierhttp://hdl.handle.net/10722/222609
ISSN
2015 Impact Factor: 3.825
2015 SCImago Journal Rankings: 2.465

 

DC FieldValueLanguage
dc.contributor.authorInouye, Karen-
dc.contributor.authorShum, Kathy-
dc.contributor.authorChan, Owen-
dc.contributor.authorMathoo, Julian-
dc.contributor.authorMatthews, Stephen G.-
dc.contributor.authorVranic, Mladen-
dc.date.accessioned2016-01-19T03:36:32Z-
dc.date.available2016-01-19T03:36:32Z-
dc.date.issued2002-
dc.identifier.citationAmerican Journal of Physiology - Endocrinology and Metabolism, 2002, v. 282, n. 6 45-6, p. E1369-E1379-
dc.identifier.issn0193-1849-
dc.identifier.urihttp://hdl.handle.net/10722/222609-
dc.description.abstractTo understand the mechanisms whereby recurrent hypoglycemia increases the risk of subsequent hypoglycemia, it was necessary to differentiate the effects of recurrent hyperinsulinemia from those of hyperinsulinemic hypoglycemia. We examined basal and hypoglycemic endocrine function in normal rats, streptozotocin-diabetic controls, and diabetic rats exposed to 4 days of 2 episodes/day of hyperinsulinemic hypoglycemia (DH) or hyperinsulinemic hyperglycemia (DI). DH and DI rats differentiated the effects of hyperinsulinemia from those of hypoglycemia. In diabetic controls, basal plasma ACTH tended to be increased, and plasma corticosterone, plasma somatostatin, and pancreatic prosomatostatin and proglucagon mRNA were increased (P < 0.05) vs. normal rats. These parameters were normalized in DH and DI rats. In diabetic controls, glucagon, epinephrine, norepinephrine, corticosterone, and peak glucose production responses to hypoglycemia were reduced (P < 0.05) vs. normal rats. In DI rats, epinephrine responses were normalized. Conversely, DH rats displayed marked further impairment of epinephrine and glucose production responses and increased peripheral insulin sensitivity (P < 0.05 vs. diabetic controls). Both insulin regimens partially normalized glucagon and fully normalized norepinephrine and corticosterone responses. In summary, recurrent hyperinsulinemia in diabetic rats normalized most pituitary-adrenal, sympathoadrenal, and pancreatic parameters. However, concurrent hypoglycemia further impaired epinephrine and glucose production responses and increased insulin sensitivity. We conclude that 1) recurrent hypoglycemia may increase the risk of subsequent hypoglycemia by increasing insulin sensitivity, and 2) epinephrine counterregulation is particularly sensitive to impairment by recurrent hypoglycemia.-
dc.languageeng-
dc.relation.ispartofAmerican Journal of Physiology - Endocrinology and Metabolism-
dc.subjectGlucose production-
dc.subjectInsulin sensitivity-
dc.subjectHypoglycemic glucose clamp-
dc.subjectEpinephrine-
dc.titleEffects of recurrent hyperinsulinemia with and without hypoglycemia on counterregulation in diabetic rats-
dc.typeArticle-
dc.description.natureLink_to_subscribed_fulltext-
dc.identifier.pmid12006368-
dc.identifier.scopuseid_2-s2.0-0036084145-
dc.identifier.volume282-
dc.identifier.issue6 45-6-
dc.identifier.spageE1369-
dc.identifier.epageE1379-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats