ArticleCellular and molecular life sciences : CMLS2017
BACE2 suppression promotes β-cell survival and function in a model of type 2 diabetes induced by human islet amyloid polypeptide overexpression.
Article in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Trial
- Significantly altered peripheral blood cell DNA methylation profile as a result of immediate effect of metformin use in healthy individuals.Clinical epigenetics · 2018Trial
- Elevated circulating BACE2 captures chronic glycemic burden and enhances the clinical identification of type 2 diabetes.iScience · 2026Article
- The human endogenous retroviral envelope HEMO protein interacts with BACE2: Novel partnership acquired in the primate lineage.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Genetics of glucose homeostasis in pregnancy and postpartum.Diabetologia · 2024Article
- BACE2 suppression in mice aggravates the adverse metabolic consequences of an obesogenic diet.Molecular metabolism · 2021Article
- The β-Secretase BACE1 in Alzheimer's Disease.Biological psychiatry · 2021Review
- Genetic discovery and risk characterization in type 2 diabetes across diverse populations.HGG advances · 2021Article
- Proteostasis of Islet Amyloid Polypeptide: A Molecular Perspective of Risk Factors and Protective Strategies for Type II Diabetes.Chemical reviews · 2021Review
- Epigenetic Alterations Are Associated With Gastric Emptying Disturbances in Diabetes Mellitus.Clinical and translational gastroenterology · 2020Observational
- Article
- Obesity-associated exosomal miRNAs modulate glucose and lipid metabolism in mice.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Hepatitis B X-interacting protein promotes the formation of the insulin gene-transcribing protein complex Pdx-1/Neurod1 in animal pancreatic β-cells.The Journal of biological chemistry · 2018Article
- BACE2 distribution in major brain cell types and identification of novel substrates.Life science alliance · 2018Article
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6 authors at 3 institutions in 1 country.
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Abstract
BACE2 (β-site APP-cleaving enzyme 2) is a protease expressed in the brain, but also in the pancreas, where it seems to play a physiological role. Amyloidogenic diseases, including Alzheimer's disease and type 2 diabetes (T2D), share the accumulation of abnormally folded and insoluble proteins that interfere with cell function. In T2D, islet amyloid polypeptide (IAPP) deposits have been shown to be a pathogenic key feature of the disease. The aim of the present study was to investigate the effect of BACE2 modulation on β-cell alterations in a mouse model of T2D induced by IAPP overexpression. Heterozygous mice carrying the human transcript of IAPP (hIAPP-Tg) were used as a model to study the deleterious effects of IAPP upon β-cell function. These animals showed glucose intolerance and impaired insulin secretion. When crossed with BACE2-deficient mice, the animals presented a significant improvement in glucose tolerance accompanied with an enhanced insulin secretion, as compared to hIAPP-Tg mice. BACE2 deficiency also partially reverted gene expression changes observed in islets from hIAPP-Tg mice, including a set of genes related to inflammation. Moreover, homozygous hIAPP mice presented a severe hyperglycemia and a high lethality rate from 8 weeks onwards due to a massive destruction of β-cell mass. This process was significantly reduced when crossed with the BACE2-KO model, improving the survival rate of the animals. Altogether, the absence of BACE2 ameliorates glucose tolerance defects induced by IAPP overexpression in the β-cell and promotes β-cell survival. Thus, targeting BACE2 may represent a promising therapeutic strategy to improve β-cell function in T2D.
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