ArticleThe Journal of clinical investigation2015
Ankyrin-B metabolic syndrome combines age-dependent adiposity with pancreatic β cell insufficiency.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 28 citations in OpenAlex.
- A Novel Mechanism for Human Cardiac Ankyrin-B Syndrome due to Reciprocal Chromosomal Translocation.Heart, lung & circulation · 2017Trial
- Ankyrin-B modulates mitochondrial fission in skeletal muscle and is required for optimal endurance exercise capacity.Nature communications · 2025Article
- Ankyrin-B is required for the establishment and maintenance of lens cytoarchitecture, mechanics and clarity.Journal of cell science · 2024Article
- Exploring protein relative relations in skeletal muscle proteomic analysis for insights into insulin resistance and type 2 diabetes.Scientific reports · 2024Article
- Mechanisms underlying the role of ankyrin-B in cardiac and neurological health and disease.Frontiers in cardiovascular medicine · 2022Review
- Giant ankyrin-B mediates transduction of axon guidance and collateral branch pruning factor sema 3A.eLife · 2021Article
- Ankyrin B and Ankyrin B variants differentially modulate intracellular and surface Cav2.1 levels.Molecular brain · 2019Article
- Article
- Expression analysis of candidate genes for fatty acid composition in adipose tissue and identification of regulatory regions.Scientific reports · 2018Article
- Calpain inhibition ameliorates scald burn-induced acute lung injury in rats.Burns & trauma · 2018Article
- Cell-autonomous adiposity through increased cell surface GLUT4 due to ankyrin-B deficiency.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Developmental pathways to adiposity begin before birth and are influenced by genotype, prenatal environment and epigenome.BMC medicine · 2017Article
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
Rare functional variants of ankyrin-B have been implicated in human disease, including hereditary cardiac arrhythmia and type 2 diabetes (T2D). Here, we developed murine models to evaluate the metabolic consequences of these alterations in vivo. Specifically, we generated knockin mice that express either the human ankyrin-B variant R1788W, which is present in 0.3% of North Americans of mixed European descent and is associated with T2D, or L1622I, which is present in 7.5% of African Americans. Young AnkbR1788W/R1788W mice displayed primary pancreatic β cell insufficiency that was characterized by reduced insulin secretion in response to muscarinic agonists, combined with increased peripheral glucose uptake and concomitantly increased plasma membrane localization of glucose transporter 4 (GLUT4) in skeletal muscle and adipocytes. In contrast, older AnkbR1788W/R1788W and AnkbL1622I/L1622I mice developed increased adiposity, a phenotype that was reproduced in cultured adipocytes, and insulin resistance. GLUT4 trafficking was altered in animals expressing mutant forms of ankyrin-B, and we propose that increased cell surface expression of GLUT4 in skeletal muscle and fatty tissue of AnkbR1788W/R1788W mice leads to the observed age-dependent adiposity. Together, our data suggest that ankyrin-B deficiency results in a metabolic syndrome that combines primary pancreatic β cell insufficiency with peripheral insulin resistance and is directly relevant to the nearly one million North Americans bearing the R1788W ankyrin-B variant.
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