Glucose Stimulation Induces Dynamic Change of Mitochondrial Morphology to Promote Insulin Secretion in the Insulinoma Cell Line INS-1E
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Fission and fusion of mitochondrial tubules are the major processes regulating mitochondrial morphology. However, the physiological significance of mitochondrial shape change is poorly understood. Glucose-stimulated insulin secretion (GSIS) in pancreatic β-cells requires mitochondrial ATP production which evokes Ca(2+) influx through plasma membrane depolarization, triggering insulin vesicle exocytosis. Therefore, GSIS reflects mitochondrial function and can be used for evaluating functional changes associated with morphological alterations of mitochondria. Using the insulin-secreting cell line INS-1E, we found that glucose stimulation induced rapid mitochondrial shortening and recovery. Inhibition of mitochondrial fission through expression of the dominant-negative mutant DLP1-K38A eliminated this dynamic mitochondrial shape change and, importantly, blocked GSIS. We found that abolishing mitochondrial morphology change in glucose stimulation increased the mitochondrial inner membrane proton leak, and thus significantly diminished the mitochondrial ATP producing capacity in response to glucose stimulation. These results demonstrate that dynamic change of mitochondrial morphology is a previously unrecognized component for metabolism-secretion coupling of pancreatic β-cells by participating in efficient ATP production in response to elevated glucose levels.
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In the rat insulinoma cell line INS-1E and in primary mouse and rat pancreatic beta cells, use of FCCP/CCCP inhibits glucose-stimulated insulin release (GSIS).
“In the rat insulinoma cell line INS-1E and in primary mouse and rat pancreatic beta cells, use of FCCP/CCCP inhibits glucose-stimulated insulin release (GSIS) [168,169,170].”
From Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases (2019) · cites this paper as [168]
In rat insulinoma cells and primary mouse and rat pancreatic beta cells, FCCP/CCCP inhibits glucose-stimulated and Ca2+-dependent insulin release.
“In rat insulinoma cells and primary mouse and rat pancreatic beta cells, FCCP/CCCP inhibits glucose-stimulated (and Ca2+-dependent) insulin release (GSIS) [168,169,170].”
From Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases (2019) · cites this paper as [168]
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- Authors
- Jhun, B. S., Lee, H., Jin, Z.-G., & Yoon, Y.
- Affiliations
- Thomas Jefferson University (US)
- Augusta University (US)
- University of Rochester Medicine (US)
- Corresponding author
- Yoon, Yisang
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2013-04-02
- Volume
- 8
- Issue
- 4
- Pages
- e60810
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3614983
- OpenAlex
- W2092479957
- Cited by
- 49
- References
- 48
- Citations by year
- 2026: 4 · 2024: 4 · 2023: 2 · 2022: 4 · 2021: 4 · 2020: 2 · 2019: 5 · 2018: 4 · 2017: 4 · 2016: 4 · 2015: 5 · 2014: 3 · 2013: 4
- FWCI
- 5.26
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- The Medicine Forum (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- American Diabetes Association
- University of Rochester
- National Institutes of Health (DK061991)
- Medical Center, University of Rochester
- National Heart, Lung, and Blood Institute (HL080611, R01HL080611)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK078618, DK-061991, DK 078618, R01DK061991)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- glucose-stimulated insulin secretion, mitochondrial morphology, mitochondrial fission, mitochondrial fusion, INS-1E cells, pancreatic beta cells, mitochondrial ATP production, mitochondrial tubules
- MeSH terms
- Insulin Secretion, Adenosine Triphosphate, Calcium, Glucose, Humans, Insulin, Insulinoma, Cell Line, Tumor
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