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Article type: Short Communication
Authors: Arrieta-Cruz, Isabela; b; 1 | Knight, Colette M.a | Gutiérrez-Juárez, Roger*
Affiliations: [a] Department of Medicine and Diabetes Research Center, Albert Einstein College of Medicine, Yeshiva University, Bronx, NY, USA | [b] Department of Basic Research, National Institute of Geriatrics, Ministry of Health, Mexico City, Mexico
Correspondence: [*] Correspondence to: Roger Gutiérrez-Juárez, MD, PhD, Department of Medicine and Diabetes Research Center, Albert Einstein College of Medicine, Jack & Pearl Resnick Campus, 1300 Morris Park Avenue, Bronx, NY 10461, USA. Tel.: +1 718 409 1925; Fax: +1 718 430 8557; roger.gutierrez@einstein.yu.edu
Note: [1] Current address: Department of Basic Research, National Institute of Geriatrics, Ministry of Health, Mexico City, Mexico.
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.
Keywords: Alzheimer’s disease, amyloid-β, diabetes, glucose homeostasis, hyperglycemia, mediobasal hypothalamus
DOI: 10.3233/JAD-131865
Journal: Journal of Alzheimer's Disease, vol. 46, no. 4, pp. 843-848, 2015
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