Evidence map›Paper›PMID 31957256›Full record

ArticleJournal of diabetes investigation2020

Characterization of the taste receptor-related G-protein, α-gustducin, in pancreatic β-cells.

Haruhide Udagawa, Masaki Hiramoto, Miho Kawaguchi, Takashi Uebanso, Mica Ohara-Imaizumi, Takao Nammo, Wataru Nishimura, Kazuki Yasuda

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 33% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 8 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 1 country.

Haruhide UdagawaDepartment of Metabolic Disorder, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.ORCID https://orcid.org/0000-0002-1425-0997
Masaki HiramotoDepartment of Biochemistry, Tokyo Medical University, Tokyo, Japan.
Miho KawaguchiDepartment of Metabolic Disorder, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Takashi UebansoDepartment of Preventive Environment and Nutrition, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, Japan.
Mica Ohara-ImaizumiDepartment of Cellular Biochemistry, Kyorin University School of Medicine, Tokyo, Japan.
Takao NammoDepartment of Metabolic Disorder, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Wataru NishimuraDepartment of Molecular Biology, International University of Health and Welfare School of Medicine, Chiba, Japan.
Kazuki YasudaDepartment of Metabolic Disorder, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.ORCID https://orcid.org/0000-0002-6966-496X
Kyorin University · JPNational Center for Global Health and Medicine · JPJichi Medical University · JPTokushima University · JPTokyo Medical University · JP

Funding

Japan Science and Technology Agency 16K16614Japan Science and Technology Agency 19K09013Japan Science and Technology Agency 21390283National Center for Global Health and Medicine 22S203National Center for Global Health and Medicine 27S6001National Center for Global Health and Medicine 28S1201National Center for Global Health and Medicine 30S1012Realization of Individually Optimized Medical Treatment for the Diseases Related to Metabolic Syndrome 13418692
6 · The paper itself

Abstract

AIMS/

introductionTaste receptors, T1rs and T2rs, and the taste-selective G-protein, α-gustducin, are expressed outside the taste-sensing system, such as enteroendocrine L cells. Here, we examined whether α-gustducin also affects nutrition sensing and insulin secretion by pancreatic β-cells. MATERIALS AND

methodsThe expression of α-gustducin and taste receptors was evaluated in β-cell lines, and in rat and mouse islets either by quantitative polymerase chain reaction or fluorescence immunostaining. The effects of α-gustducin knockdown on insulin secretion and on cyclic adenosine monophosphate and intracellular Ca

resultsThe expression of Tas1r3 and α-gustducin was confirmed in β-cell lines and pancreatic islets. Basal levels of cyclic adenosine monophosphate, intracellular calcium and insulin secretion were significantly enhanced with α-gustducin knockdown in INS-1 cells. The expression of α-gustducin was decreased in high-fat diet-fed mice and in diabetic db/db mice. Sucralose-induced insulin secretion was not attenuated in INS-1 cells with α-gustducin knockdown or in mouse islets with decreased expression of α-gustducin.

conclusionsα-Gustducin is involved in the regulation of cyclic adenosine monophosphate, intracellular calcium levels and insulin secretion in pancreatic β-cells in a manner independent of taste receptor signaling. α-Gustducin might play a novel role in β-cell physiology and the development of type 2 diabetes.

Indexed as

AnimalsCell LineCyclic AMPDisease Models, AnimalHumansInsulin-Secreting CellsInsulin SecretionIntracellular Calcium-Sensing ProteinsIslets of LangerhansMiceRatsReceptors, G-Protein-CoupledSignal TransductionTaste Receptors, Type 2TransducinCyclic AMPgustducinIntracellular Calcium-Sensing ProteinsReceptors, G-Protein-Coupledtaste receptors, type 1Taste Receptors, Type 2TransducinInsulin secretionTaste receptorα-Gustducin

Identifiers

PMID31957256
PMCPMC7378449
OpenAlexW3002427401

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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.