Palmitate-induced impairment of glucose-stimulated insulin secretion precedes mitochondrial dysfunction in mouse pancreatic islets
Open accessAbstract
It has been well established that excessive levels of glucose and palmitate lower glucose-stimulated insulin secretion (GSIS) by pancreatic β-cells. This β-cell ‘glucolipotoxicity’ is possibly mediated by mitochondrial dysfunction, but involvement of bioenergetic failure in the pathological mechanism is the subject of ongoing debate. We show in the present study that increased palmitate levels impair GSIS before altering mitochondrial function. We demonstrate that GSIS defects arise from increased insulin release under basal conditions in addition to decreased insulin secretion under glucose-stimulatory conditions. Real-time respiratory analysis of intact mouse pancreatic islets reveals that mitochondrial ATP synthesis is not involved in the mechanism by which basal insulin is elevated. Equally, mitochondrial lipid oxidation and production of reactive oxygen species (ROS) do not contribute to increased basal insulin secretion. Palmitate does not affect KCl-induced insulin release at a basal or stimulatory glucose level, but elevated basal insulin release is attenuated by palmitoleate and associates with increased intracellular calcium. These findings deepen our understanding of β-cell glucolipotoxicity and reveal that palmitate-induced GSIS impairment is disconnected from mitochondrial dysfunction, a notion that is important when targeting β-cells for the treatment of diabetes and when assessing islet function in human transplants.
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Whatever role glucolipotoxicity may have in impairing GSIS in T2D is disconnected from mitochondrial dysfunction.
“From the observations of this study, it seems that whatever role glucolipotoxicity may have in impairing GSIS in T2D is disconnected from mitochondrial dysfunction, which is surprising given the role of the mitochondria in ATP and reactive oxygen species (ROS) generation needed for both phases of insulin secretion.174,175”
From A review of current trends with type 2 diabetes epidemiology, aetiology, pathogenesis, treatments and future perspectives (2021) · cites this paper as [173]
Impaired GSIS observed in vitro with INS-1E cells exposed to glucolipotoxicity (palmitate + high glucose) is not dependent on mitochondrial dysfunction.
“Interestingly, they have found that the impaired GSIS observed during in vitro studies involving exposing pancreatic beta-cell line INS-1E to glucolipotoxicity conditions (palmitate + high glucose) was found not to be dependent on mitochondrial dysfunction.173”
From A review of current trends with type 2 diabetes epidemiology, aetiology, pathogenesis, treatments and future perspectives (2021) · cites this paper as [173]
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- Authors
- Barlow, J., Jensen, V. H., Jastroch, M., & Affourtit, C.
- Affiliations
- University of Plymouth (GB)
- School of Biomedical and Healthcare Sciences, Plymouth University, Drake Circus, Plymouth PL4 8AA, U.K.
- Helmholtz Diabetes Center and Institute for Diabetes and Obesity, Garching, Parkring 13, Garching D-85748, Germany
- Corresponding author
- Barlow, Jonathan
- Affourtit, Charles
- Venue
- Biochemical Journal
- Publisher
- Portland Press Ltd.
- Published
- 2016-02-09
- Volume
- 473
- Issue
- 4
- Pages
- 487-496
- ISSN
- 0264-6021 (ISSN-L)
- 1470-8728
- OpenAlex
- W2228066206
- Cited by
- 45
- References
- 43
- Citations by year
- 2025: 3 · 2024: 1 · 2023: 3 · 2022: 2 · 2021: 4 · 2020: 7 · 2019: 5 · 2018: 9 · 2017: 8 · 2016: 3
- FWCI
- 6.74
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Locations
- Biochemical Journal (publishedVersion)
- PubMed (publishedVersion)
- PEARL (University of Plymouth) (submittedVersion)
- Site cant be reached (submittedVersion)
- Funders
- University of Exeter
- Medical Research Council (G1100165)
- Helmholtz Zentrum München
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- palmitate, glucose-stimulated insulin secretion, pancreatic beta cells, glucolipotoxicity, mitochondrial dysfunction, basal insulin secretion, mitochondrial ATP production, reactive oxygen species, palmitoleic acid, intracellular calcium, diabetes mellitus, islet transplantation
- MeSH terms
- Insulin Secretion, Animals, Cell Line, Female, Glucose, Insulin, Islets of Langerhans, Male, Mice, Inbred C57BL, Mitochondria, Palmitic Acid, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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