CoChat
Sign Up
Cited by 258Pancreatic function and diabetesDiabetes Treatment and ManagementDiabetes and associated disorders

The DOI matches its Crossref record; 53 of the 53 references it cites were found in a registry or an index.

Glucose‐stimulated insulin secretion: A newer perspective

Open access
Komatsu, Mitsuhisa, Takei, Masahiro, Ishii, Hiroaki, Sato, Yoshihiko·2013·Journal of Diabetes Investigation
DOI 10.1111/jdi.12094PMC PMC4020243
Open this paper in CoChat — free accountOpen PDF

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 (K ATP channel)‐dependent mechanism, which is gradually augmented in a K ATP 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 K ATP channels. Robust GSIS in patients with a loss of function mutation of the sulfonylurea receptor, a subunit of K ATP 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 K ATP channel‐ and Ca 2+‐independent manner. We hypothesize that GSIS occurs in islet β‐cells without glucose regulation of K ATP 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.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1111/jdi.12094

Cites

53 of 53 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 51 references

Research works printed but not linked: 1

  1. 10.1172/JCI200522955 · DOI

Cited by

Sorted by citations

Items 201–258 of 258

Related

See all

Metadata

Authors
Komatsu, M., Takei, M., Ishii, H., & Sato, Y.
Affiliations
Shinshu University (JP)
Corresponding author
Komatsu, Mitsuhisa
ORCID
Venue
Journal of Diabetes Investigation
Publisher
Wiley
Published
2013-05-15
Volume
4
Issue
6
Pages
511-516
ISSN
  • 2040-1116 (ISSN-L)
  • 2040-1124
DOI
10.1111/jdi.12094
PMC
PMC4020243
OpenAlex
W1989817905
Cited by
256
References
51
Citations by year
2026: 6 · 2025: 25 · 2024: 25 · 2023: 27 · 2022: 29 · 2021: 26 · 2020: 26 · 2019: 17 · 2018: 23 · 2017: 14 · 2016: 13 · 2015: 18 · 2014: 7
FWCI
2.36
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • Journal of Diabetes Investigation (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
Japan Society for the Promotion of Science (21591128, 25461383)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
Keywords
glucose-stimulated insulin secretion, pancreatic beta cells, ATP-sensitive potassium channels, sulfonylurea receptor, glucagon-like peptide-1, parasympathetic activation, free fatty acids, amino acids, cyclic AMP, protein kinase C, protein kinase A, biphasic insulin secretion, loss-of-function mutations, postprandial blood glucose

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 ›

Are you an author, or do you see a problem with this page? Request a review