In a study appearing in the June issue of the Journal of Clinical Investigation, Rory J. McCrimmon and colleagues from Yale University, show that administration to the brain of urocortin I suppresses the counterregulatory response to hypoglycemia for at least 24 hours in rats. They show that urocortin I, which activates corticotrophin-releasing factor receptor 2 (CRFR2), impairs the sensitivity of glucose-sensing neurons in the brain. In contrast, administration of CRF, which activates CRFR1, amplifies the response to hypoglycemia. The data suggest that the regulation of the counterregulatory response to hypoglycemia is largely determined by the interaction between CRFR2-mediated suppression and CRFR1-mediated activation in the hypothalamus.
In an accompanying commentary, Philip Cryer from Washington University School of Medicine discusses how hypoglycemia in diabetes will likely remain a problem until safe and effective methods are developed that would offer insulin replacement based on plasma glucose concentration.
TITLE: Corticotrophin-releasing factor receptors within the ventromedial hypothalamus regulate hypoglycemia-induced hormonal counterregulation
Rory J. McCrimmon
Yale University, New Haven, Connecticut, USA.
Phone: (203) 785-4664; Fax: (203) 737-5558; E-mail: firstname.lastname@example.org.
View the PDF of this article at: https://www.the-jci.org/article.php?id=27775
TITLE: Mechanisms of sympathoadrenal failure and hypoglycemia in diabetes
Philip E. Cryer
Washington University School of Medicine, St. Louis, Missouri, USA.
Phone: (314) 362-7635; Fax: (314) 362-7989; E-mail: email@example.com.
View the PDF of this article at: https://www.the-jci.org/article.php?id=28735
Last reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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