Evidence map›Paper›PMID 33952814›Full record

ArticleInternal medicine (Tokyo, Japan)2021

The Amount of Residual Incretin Regulates the Pancreatic β-cell Function and Glucose Homeostasis.

Tatsuya Kondo, Sayaka Kitano, Nobukazu Miyakawa, Takuro Watanabe, Rieko Goto, Miki Sato, Satoko Hanatani, Masaji Sakaguchi, Motoyuki Igata, Junji Kawashima and 3 more

Open access · diamondAbstract readCase Reports
In one paragraph

Article in Internal medicine (Tokyo, Japan), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 51% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Article
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

13 authors at 2 institutions in 1 country.

Tatsuya KondoDepartment of Diabetes, Metabolism and Endocrinology, Kumamoto University Hospital, Japan.
Sayaka KitanoDepartment of Diabetes, Metabolism and Endocrinology, Kumamoto University Hospital, Japan.
Nobukazu MiyakawaDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Japan.
Takuro WatanabeDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Japan.
Rieko GotoDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Japan.
Miki SatoDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Japan.
Satoko HanataniDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Japan.
Masaji SakaguchiDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Japan.
Motoyuki IgataDepartment of Diabetes, Metabolism and Endocrinology, Kumamoto University Hospital, Japan.
Junji KawashimaDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Japan.
Hiroyuki MotoshimaDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Japan.
Takeshi MatsumuraDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Japan.
Eiichi ArakiDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Japan.
Kumamoto University · JPKumamoto University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The gastrointestinal tract is considered an important endocrine organ for controlling glucose homeostasis via the production of incretins. A 21-year-old man emergently underwent total colectomy due to severe ulcerative colitis, and overt diabetes became evident. Weekly administration of a glucagon-like peptide (GLP)-1 receptor agonist (RA) dramatically improved his glucose control. Levels of GLP-1 or gastric inhibitory polypeptide (GIP) were low at the baseline in the duodenum and serum of the patient. After 11 months of GLP-1RA treatment, his HbA1c worsened again, and intensive insulin therapy was necessary to control his glucose levels. Our report may explain the significance of residual incretin for maintaining the pancreatic β-cell function.

Indexed as

Diabetes Mellitus, Type 2IncretinsAdultBlood GlucoseGastric Inhibitory PolypeptideGlucoseHomeostasisHumansInsulinMaleYoung AdultBlood GlucoseGastric Inhibitory PolypeptideGlucoseIncretinsInsulincolectomydiabetesgastric inhibitory polypeptide (GIP)glucagon-like peptide (GLP)-1

Identifiers

PMID33952814
PMCPMC8170253
OpenAlexW3157127377

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.