Metabolic Signaling in Fuel-Induced Insulin Secretion
Open accessAbstract
The pancreatic islet β cell senses circulating levels of calorigenic nutrients to secrete insulin according to the needs of the organism. Altered insulin secretion is linked to various disorders such as diabetes, hypoglycemic states, and cardiometabolic diseases. Fuel stimuli, including glucose, free fatty acids, and amino acids, promote insulin granule exocytosis primarily via their metabolism in β cells and the production of key signaling metabolites. This paper reviews our current knowledge of the pathways involved in both positive and negative metabolic signaling for insulin secretion and assesses the role of established and candidate metabolic coupling factors, keeping recent developments in focus.
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Almost all glucose entering glycolysis proceeds into the Krebs cycle in β-cells.
“An important aspect of glucose metabolism in the β-cell is that almost all the glucose entering glycolysis proceeds into the Krebs cycle (602) (520).”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [520]
The passage labeled Abstract says that glucose carbons are largely converted to pyruvate, which is primarily used in the citric acid cycle. This supports the pathway described, but does not establish the stronger claim that almost all glucose entering glycolysis proceeds into that cycle. (LLM, conf=0.84)
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- Authors
- Prentki, M., Matschinsky, F. M., & Madiraju, S. R. M.
- Affiliations
- Centre Hospitalier de l’Université de Montréal (CA)
- Corresponding author
- Prentki, Marc
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2013-08
- Volume
- 18
- Issue
- 2
- Pages
- 162-185
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W1973045246
- Cited by
- 548
- References
- 14
- Citations by year
- 2026: 24 · 2025: 36 · 2024: 48 · 2023: 37 · 2022: 50 · 2021: 42 · 2020: 44 · 2019: 42 · 2018: 34 · 2017: 47 · 2016: 58 · 2015: 49 · 2014: 32 · 2013: 5
- FWCI
- 8.55
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 370 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (19525, 22122)
- Canadian Institutes of Health Research
- National Health Research Institutes
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- insulin secretion, pancreatic beta cells, metabolic signaling, glucose, free fatty acids, amino acids, insulin granule exocytosis, diabetes mellitus, hypoglycemia, cardiometabolic disease
- MeSH terms
- Insulin Secretion, Amino Acids, Blood Glucose, Diabetes Mellitus, Energy Metabolism, Fatty Acids, Nonesterified, Glucose, Humans, Insulin, Signal Transduction, Insulin-Secreting Cells
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