ReviewInternational journal of molecular sciences2025
Stimulus-Secretion Coupling Mechanisms of Glucose-Induced Insulin Secretion: Biochemical Discrepancies Among the Canonical, ADP Privation, and GABA-Shunt Models.
Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- GABA Regulates CaMetabolites · 2026Article
- The Dual Anaplerotic Model (DAM): Integral Roles of Pyruvate Carboxylase and the GABA Shunt in Beta Cell Insulin Secretion.Life (Basel, Switzerland) · 2026Article
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Authors and funding
1 author.
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Abstract
Integration of old and recent experimental data consequences is needed to correct and help improve the hypothetical mechanism responsible for the stimulus-secretion coupling mechanism of glucose-induced insulin secretion. The main purpose of this review is to supply biochemical considerations about some of the metabolic pathways implicated in the process of insulin secretion. It is emphasized that glucose β-cells' threshold to activate secretion (5 mM) might depend on the predominance of anaerobic glycolysis at this basal glucose concentration. This argues against the predominance of phosphoenolpyruvate (PEP) over mitochondrial pyruvate oxidation for the initiation of insulin secretion. Full quantitative and qualitative reproduction, except the threshold effect, of glucose-induced insulin release by a permeable methylated analog of succinic acid indicates that mitochondrial metabolism is enough for sustained insulin secretion. Mitochondrial PEP generation is skipped if the GABA-shunt pathway is exclusively coupled to the citric acid cycle, as proposed in the "GABA-shunt" model of stimulus-secretion coupling. Strong or maintained depolarization by KCl or sulfonylureas might induce the opening of β-cells Cx36 hemichannels, allowing the loss of adenine nucleotides and other metabolites, mimicking the effect of an excessive mitochondrial ATP demand. A few alterations of OxPhos (Oxidative Phosphorylation) regulation in human T2D islets have been described, but the responsible mechanism(s) is (are) not yet known. Finally, some experimental data arguing as proof of the relative irrelevance of the mitochondrial function in the insulin secretion coupling mechanism for the initiation and/or sustained stimulation of hormone release are discussed.
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Registered trials
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