Acute Exposure of the Mediobasal Hypothalamus to Amyloid-β25-35 Perturbs Hepatic Glucose Metabolism

Isabel Arrieta-Cruz, Colette M. Knight, Roger Gutiérrez-Juárez

Research output: Contribution to journalArticle

7 Scopus citations

Abstract

Patients with Alzheimer's disease (AD) have a higher risk for developing insulin resistance and diabetes. Amyloid plaques, a hallmark of AD, are composed of amyloid-β (Aβ). Because the mediobasal hypothalamus controls hepatic glucose production, we examined the hypothesis that its exposure to Aβ perturbs the regulation of glucose metabolism. The infusion of Aβ25-35, but not its scrambled counterpart, into the mediobasal hypothalamus of young rats, increased circulating glucose as a consequence of enhanced hepatic glucose production during pancreatic clamp studies. These findings suggest a link between AD and alterations of glucose metabolism.

Original languageEnglish (US)
Pages (from-to)843-848
Number of pages6
JournalJournal of Alzheimer's Disease
Volume46
Issue number4
DOIs
StatePublished - Jun 26 2015

Keywords

  • Alzheimer's disease
  • amyloid-β
  • diabetes
  • glucose homeostasis
  • hyperglycemia
  • mediobasal hypothalamus

ASJC Scopus subject areas

  • Neuroscience(all)
  • Clinical Psychology
  • Geriatrics and Gerontology
  • Psychiatry and Mental health

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