Acute exposure of the mediobasal hypothalamus to amyloid-β<inf>25-35</inf> perturbs hepatic glucose metabolism

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

Research output: Contribution to journalArticle

7 Citations (Scopus)

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 Aβ<inf>25-35</inf>, 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

Fingerprint

Amyloid
Hypothalamus
Glucose
Liver
Alzheimer Disease
Amyloid Plaques
Insulin Resistance

Keywords

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

ASJC Scopus subject areas

  • Psychiatry and Mental health
  • Geriatrics and Gerontology
  • Clinical Psychology

Cite this

Acute exposure of the mediobasal hypothalamus to amyloid-β<inf>25-35</inf> perturbs hepatic glucose metabolism. / Arrieta-Cruz, Isabel; Knight, Colette M.; Gutiérrez-Juárez, Roger.

In: Journal of Alzheimer's Disease, Vol. 46, No. 4, 26.06.2015, p. 843-848.

Research output: Contribution to journalArticle

Arrieta-Cruz, Isabel ; Knight, Colette M. ; Gutiérrez-Juárez, Roger. / Acute exposure of the mediobasal hypothalamus to amyloid-β<inf>25-35</inf> perturbs hepatic glucose metabolism. In: Journal of Alzheimer's Disease. 2015 ; Vol. 46, No. 4. pp. 843-848.
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