Evidence map›Paper›PMID 36312739›Full record

ArticleJournal of ginseng research2022

Compound K attenuates hyperglycemia by enhancing glucagon-like peptide-1 secretion through activating TGR5 via the remodeling of gut microbiota and bile acid metabolism.

Fengyuan Tian, Shuo Huang, Wangda Xu, Lan Chen, Jianming Su, Haixiang Ni, Xiaohong Feng, Jie Chen, Xi Wang, Qi Huang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of ginseng research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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

26 citing papers in PubMed.

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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

10 authors.

Fengyuan TianFirst School of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Shuo HuangFirst School of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Wangda XuFirst School of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Lan ChenFirst School of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Jianming SuDepartment of Emergency, First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Haixiang NiDepartment of Endocrinology, First Affiliated Hospital of Zhejiang Chinese Medicine University, Hangzhou, China.
Xiaohong FengDepartment of Endocrinology, First Affiliated Hospital of Zhejiang Chinese Medicine University, Hangzhou, China.
Jie ChenDepartment of Endocrinology, First Affiliated Hospital of Zhejiang Chinese Medicine University, Hangzhou, China.
Xi WangCentral Laboratory, First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.
Qi HuangDepartment of Endocrinology, First Affiliated Hospital of Zhejiang Chinese Medicine University, Hangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Incretin impairment, characterized by insufficient secretion of L-cell-derived glucagon-like peptide-1 (GLP-1), is a defining step of type 2 diabetes mellitus (T2DM). Ginsenoside compound K (CK) can stimulate GLP-1 secretion; however, the potential mechanism underlying this effect has not been established. Methods: CK (40 mg/kg) was administered orally to male db/db mice for 4 weeks. The body weight, oral glucose tolerance, GLP-1 secretion, gut microbiota sequencing, bile acid (BA) profiles, and BA synthesis markers of each subject were then analyzed. Moreover, TGR5 expression was evaluated by immunoblotting and immunofluorescence, and L-cell lineage markers involved in L-cell abundance were analyzed. Results: CK ameliorated obesity and impaired glucose tolerance in db/db mice by altering the gut microbiota, especially Conclusions: The results indicate that CK improves glucose homeostasis by increasing L-cell numbers, which enhances GLP-1 release through a mechanism partially mediated by the gut microbiota-BA-TGR5 pathway. Therefore, that therapeutic attempts with CK might be useful for patients with T2DM.

Indexed as

Bile acidsCompound KEnteroendocrine cellsGLP-1TGR5

Identifiers

PMID36312739
PMCPMC9597441

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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.