Doc2b enrichment enhances glucose homeostasis in mice via potentiation of insulin secretion and peripheral insulin sensitivity
Open accessAbstract
Aims/hypothesis Insulin secretion from pancreatic beta cells and insulin-stimulated glucose uptake into skeletal muscle are processes regulated by similar isoforms of the soluble N-ethylmaleimide-sensitive factor-attachment protein receptor (SNARE) and mammalian homologue of unc-18 (Munc18) protein families. Double C2 domain β (Doc2b), a SNARE- and Munc18-interacting protein, is implicated as a crucial effector of glycaemic control. However, whether Doc2b is naturally limiting for these processes, and whether Doc2b enrichment might exert a beneficial effect upon glycaemia in vivo, remains undetermined. Methods Tetracycline-repressible transgenic (Tg) mice engineered to overexpress Doc2b simultaneously in the pancreas, skeletal muscle and adipose tissues were compared with wild-type (Wt) littermate mice regarding glucose and insulin tolerance, islet function in vivo and ex vivo, and skeletal muscle GLUT4 accumulation in transverse tubule/sarcolemmal surface membranes. SNARE complex formation was further assessed using Doc2b overexpressing L6-GLUT4-myc myoblasts to derive mechanisms relatable to physiological in vivo analyses. Results Doc2b Tg mice cleared glucose substantially faster than Wt mice, correlated with enhancements in both phases of insulin secretion and peripheral insulin sensitivity. Heightened peripheral insulin sensitivity correlated with elevated insulin-stimulated GLUT4 vesicle accumulation in cell surface membranes of Doc2b Tg mouse skeletal muscle. Mechanistic studies demonstrated Doc2b enrichment to enhance syntaxin-4-SNARE complex formation in skeletal muscle cells. Conclusions/interpretation Doc2b is a limiting factor in SNARE exocytosis events pertinent to glycaemic regulation in vivo. Doc2b enrichment may provide a novel means to simultaneously boost islet and skeletal muscle function in vivo in the treatment and/or prevention of diabetes.
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In neurones, Doc2a and b translocate to the plasma membrane when [Ca2+]i is elevated and promote vesicle fusion.
“In neurones, Doc2a and b translocate to the plasma membrane when [Ca2+]i is elevated (235) and promote vesicle fusion (534).”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [534]
Citation 534 is attached to the claim that Doc2a and Doc2b promote vesicle fusion. The Discussion describes a model in which Doc2b creates docking/fusion sites for GLUT4 vesicles, but this concerns skeletal muscle, not neuronal vesicle fusion, and the paper provides no comparable finding for Doc2a. The calcium-dependent translocation clause has a separate citation and is not assessed here. (LLM, conf=0.85)
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- Authors
- Ramalingam, L., Oh, E., & Thurmond, D. C.
- Affiliations
- Indiana University School of Medicine (US)
- Indiana University Indianapolis (US)
- Corresponding author
- Thurmond, Debbie C.
- Venue
- Diabetologia
- Published
- 2014-04-06
- Volume
- 57
- Issue
- 7
- Pages
- 1476-1484
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- PMC
- PMC4055500
- OpenAlex
- W1976212598
- Cited by
- 33
- References
- 41
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 2 · 2023: 3 · 2022: 3 · 2021: 3 · 2020: 2 · 2019: 2 · 2018: 3 · 2017: 5 · 2015: 1 · 2014: 4
- FWCI
- 3.31
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Syracuse University Libraries (Syracuse University) (submittedVersion, cc-by)
- IUScholarWorks (Indiana University) (submittedVersion)
- PMC
- Funders
- National Institutes of Health (5r01dk102233-08)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 076614, DK067912 AND, R01-DK-102233, R01DK076614, R01DK067912)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- DOC2B, glucose homeostasis, insulin secretion, peripheral insulin sensitivity, SNARE complex, syntaxin 4, Munc18, skeletal muscle glucose uptake, pancreatic beta cells, diabetes treatment, transgenic overexpression
- MeSH terms
- Insulin Secretion, Adipose Tissue, Animals, Calcium-Binding Proteins, Exocytosis, Glucose, Homeostasis, Insulin, Insulin Resistance, Mice, Transgenic, Nerve Tissue Proteins, Pancreas, Muscle, Skeletal, R-SNARE Proteins, Mice
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