ReviewJournal of diabetes investigation2013
Glucose-stimulated insulin secretion: A newer perspective.
Review in Journal of diabetes investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.
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Who cites it
124 citing papers in PubMed, 261 citations in OpenAlex.
- Hepatic translational rewiring in insulin deficiency identifies Reg3α as an insulin-independent glucoregulatory factor.Endocrinology · 2026Article
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- Towards curing type 1 diabetes: Prospects and challenges of allogeneic or xenogeneic donor islet cell transplantation.World journal of transplantation · 2025Review
- Local Insulin for Local Needs? Insights into Retinal Insulin Signaling and RPE Metabolism.Biomolecules · 2025Review
- Secretory stimuli distinctly regulate insulin secretory granule maturation through structural remodeling.Structure (London, England : 1993) · 2025Article
- Glucose-Stimulated Insulin Secretion via Perfusion through the Mice Vasculature with an Intact Pancreas.Journal of visualized experiments : JoVE · 2025Article
- Regulation and function of insulin and insulin-like growth factor receptor signalling.Nature reviews. Molecular cell biology · 2025Review
- Pathophysiological insights into asprosin: an emerging adipokine in reproductive health.Reviews in endocrine & metabolic disorders · 2025Review
- Re-evaluating Intra-Islet Paracrine Signaling: Precision, Pulsatility and the Path toward Mechanistic Clarity.Journal of biomedical research & environmental sciences · 2025Article
- The novel role ofJournal of diabetes and metabolic disorders · 2025Article
- Impact of the Microtubule Cytoskeleton on Insulin Transport in Beta Cells: A 3D Computational Study.bioRxiv : the preprint server for biology · 2025Article
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- Hepatic and Pancreatic Cellular Response to Early Life Nutritional Mismatch.Endocrinology · 2025Article
- Effects of the ketogenic diet on skin-potential benefits and risks.Frontiers in nutrition · 2025Review
- Light modulates glucose and lipid homeostasis via the sympathetic nervous system.Science advances · 2024Article
- Decoding Insulin Secretory Granule Maturation Using Genetically Encoded pH Sensors.ACS sensors · 2024Article
- Kinesin-1 mediates proper ER folding of the CaEMBO reports · 2024Article
- Light modulates glucose and lipid homeostasis via the sympathetic nervous system.bioRxiv : the preprint server for biology · 2024Article
64 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Existing concepts and models for glucose-stimulated insulin secretion (GSIS) are overviewed and a newer perspective has been formulated toward the physiological understanding of GSIS. A conventional model has been created on the basis of in vitro data on application of a square wave high glucose in the absence of any other stimulatory inputs. Glucose elicits rapid insulin release through an adenosine triphosphate-sensitive K(+) channel (KATP channel)-dependent mechanism, which is gradually augmented in a KATP channel-independent manner. Biphasic GSIS thus occurs. In the body, the β-cells are constantly exposed to stimulatory signals, such as glucagon-like peptide 1 (GLP-1), parasympathetic inputs, free fatty acid (FFA), amino acids and slightly suprathreshold levels of glucose, even at fasting. GLP-1 increases cellular cyclic adenosine monophosphate, parasympathetic stimulation activates protein kinase C, and FFA, amino acids and glucose generate metabolic amplification factors. Plasma glucose concentration gradually rises postprandially under such tonic stimulation. We hypothesize that these stimulatory inputs together make the β-cells responsive to glucose independently from its action on KATP channels. Robust GSIS in patients with a loss of function mutation of the sulfonylurea receptor, a subunit of KATP channels, is compatible with this hypothesis. Furthermore, pre-exposure of the islets to an activator of protein kinase A and/or C makes β-cells responsive to glucose in a KATP channel- and Ca(2+)-independent manner. We hypothesize that GSIS occurs in islet β-cells without glucose regulation of KATP channels in vivo, for which priming with cyclic adenosine monophosphate, protein kinase C and non-glucose nutrients are required. To understand the physiology of GSIS, comprehensive integration of accumulated knowledge is required.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.