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Acute hyperglycemia induced by hyperglycemic clamp affects plasma Amyloid-β in type 2 diabetes
Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.ORCID iD: 0000-0002-1341-6828
Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Section of Sustainable Health.ORCID iD: 0000-0001-8608-0168
Umeå University, Faculty of Medicine, Department of Medical and Translational Biology.
Umeå University, Faculty of Medicine, Department of Medical and Translational Biology.ORCID iD: 0000-0002-3553-7348
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2024 (English)In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 99, no 3, p. 1033-1046Article in journal (Refereed) Published
Abstract [en]

Background: Individuals with type 2 diabetes (T2D) have an increased risk of cognitive symptoms and Alzheimer's disease (AD). Mis-metabolism with aggregation of amyloid-β peptides (Aβ) play a key role in AD pathophysiology. Therefore, human studies on Aβ metabolism and T2D are warranted.

Objective: The objective of this study was to examine whether acute hyperglycemia affects plasma Aβ1-40 and Aβ1-42 concentrations in individuals with T2D and matched controls.

Methods: Ten participants with T2D and 11 controls (median age, 69 years; range, 66-72 years) underwent hyperglycemic clamp and placebo clamp (saline infusion) in a randomized order, each lasting 4 hours. Aβ1-40, Aβ1-42, and insulin-degrading enzyme (IDE) plasma concentrations were measured in blood samples taken at 0 and 4 hours of each clamp. Linear mixed-effect regression models were used to evaluate the 4-hour changes in Aβ1-40 and Aβ1-42 concentrations, adjusting for body mass index, estimated glomerular filtration rate, and 4-hour change in insulin concentration.

Results: At baseline, Aβ1-40 and Aβ1-42 concentrations did not differ between the two groups. During the hyperglycemic clamp, Aβ decreased in the control group, compared to the placebo clamp (Aβ1-40: p = 0.034, Aβ1-42: p = 0.020), IDE increased (p = 0.016) during the hyperglycemic clamp, whereas no significant changes in either Aβ or IDE was noted in the T2D group.

Conclusions: Clamp-induced hyperglycemia was associated with increased IDE levels and enhanced Aβ40 and Aβ42 clearance in controls, but not in individuals with T2D. We hypothesize that insulin-degrading enzyme was inhibited during hyperglycemic conditions in people with T2D.

Place, publisher, year, edition, pages
IOS Press, 2024. Vol. 99, no 3, p. 1033-1046
Keywords [en]
Alzheimer's disease, amyloid-β, cognition, endocrinology and metabolism specialty, hyperglycemia, type 2 diabetes
National Category
Neurosciences
Identifiers
URN: urn:nbn:se:umu:diva-225948DOI: 10.3233/JAD-230628PubMedID: 38728183Scopus ID: 2-s2.0-85194944157OAI: oai:DiVA.org:umu-225948DiVA, id: diva2:1868793
Funder
Region VästerbottenSwedish Diabetes AssociationSwedish Research Council, 2023-00356Swedish Research Council, 2022-01018Swedish Research Council, 2019-02397Swedish Research Council, 2017-00915Swedish Research Council, 2022-00732EU, Horizon Europe, 101053962Familjen Erling-Perssons StiftelseStiftelsen Gamla TjänarinnorThe Swedish Brain Foundation, FO2022-0270The Swedish Brain Foundation, FO2017-0243The Swedish Brain Foundation, ALZ2022-0006EU, Horizon 2020, 860197Alzheimerfonden, AF-930351Alzheimerfonden, AF-939721Alzheimerfonden, AF-968270Available from: 2024-06-12 Created: 2024-06-12 Last updated: 2024-07-02Bibliographically approved

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Rolandsson, OlovTornevi, AndreasSteneberg, PärEdlund, HelenaOlsson, Tommy

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Rolandsson, OlovTornevi, AndreasSteneberg, PärEdlund, HelenaOlsson, Tommy
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Family MedicineSection of Sustainable HealthDepartment of Medical and Translational BiologySection of Medicine
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