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Gαo Represses Insulin Secretion by Reducing Vesicular Docking in Pancreatic β-Cells

2010· article· en· 36 citations· W2140920227 on OpenAlex· 10.2337/db09-1719

Why is this work in the frame?

A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.

Canadian affiliationAn author listed a Canadian institution. This is the only route the usual frame has.

The three-model screen

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All three models called this out of scope.

stratum: aff_core · design weight: 5595.24 (the sample is stratified; any rate computed without the weight is wrong)
Claude Opus 4.8OUT
genre: empirical
about Canada: no
confidence: high

Molecular physiology of G-protein regulation of insulin secretion.

GPT-5.6 (high)OUT
genre: empirical
about Canada: no
confidence: high

The study examines insulin secretion and pancreatic biology, not research practice.

Grok 4.5OUT
genre: empirical
about Canada: no
confidence: high

Cell biology of G-protein regulation of insulin secretion, domain biomedical science.

Abstract

OBJECTIVE: Pertussis toxin uncoupling-based studies have shown that Gαi and Gαo can inhibit insulin secretion in pancreatic β-cells. Yet it is unclear whether Gαi and Gαo operate through identical mechanisms and how these G-protein-mediated signals inhibit insulin secretion in vivo. Our objective is to examine whether/how Gαo regulates islet development and insulin secretion in β-cells. RESEARCH DESIGN AND METHODS: Immunoassays were used to analyze the Gαo expression in mouse pancreatic cells. Gαo was specifically inactivated in pancreatic progenitor cells by pancreatic cell-specific gene deletion. Hormone expression and insulin secretion in response to different stimuli were assayed in vivo and in vitro. Electron microscope and total internal reflection fluorescence-based assays were used to evaluate how Gαo regulates insulin vesicle docking and secretion in response to glucose stimulation. RESULTS: Islet cells differentiate properly in Gαo(-/-) mutant mice. Gαo inactivation significantly enhances insulin secretion both in vivo and in isolation. Gαo nullizygous β-cells contain an increased number of insulin granules docked on the cell plasma membrane, although the total number of vesicles per β-cell remains unchanged. CONCLUSIONS: Gαo is not required for endocrine islet cell differentiation, but it regulates the number of insulin vesicles docked on the β-cell membrane.

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The record

Venue
Diabetes
Topic
Pancreatic function and diabetes
Field
Medicine
Canadian institutions
Université de Sherbrooke
Funders
National Institute of Diabetes and Digestive and Kidney DiseasesJapan Society for the Promotion of ScienceNational Institutes of HealthAstellas Foundation for Research on Metabolic DisordersVanderbilt Diabetes Research and Training Center, Vanderbilt University Medical CenterAstellas PharmaVanderbilt UniversityResearch Foundation for Opto-Science and TechnologyNational Institute of Environmental Health SciencesU.S. Department of Veterans Affairs
Keywords
InsulinSecretionBiologyIsletEndocrinologyInternal medicineIn vivoEnteroendocrine cellCell biologyHormoneEndocrine systemMedicine
Has abstract in OpenAlex
yes