Evidence map›Paper›PMID 31142783›Full record

ArticleScientific reports2019

Berberine alleviates hyperglycemia by targeting hepatic glucokinase in diabetic db/db mice.

Meng Li, Yanqi Dang, Qiong Li, Wenjun Zhou, Jianping Zuo, Zemin Yao, Li Zhang, Guang Ji

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 26 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 2 institutions in 2 countries.

Meng LiInstitute of Digestive Diseases, China-Canada Center of Research for Digestive Diseases (ccCRDD), Longhua Hospital, Shanghai University of Traditional Chinese Medicine, 200032, Shanghai, China.
Yanqi DangInstitute of Digestive Diseases, China-Canada Center of Research for Digestive Diseases (ccCRDD), Longhua Hospital, Shanghai University of Traditional Chinese Medicine, 200032, Shanghai, China.
Qiong LiInstitute of Digestive Diseases, China-Canada Center of Research for Digestive Diseases (ccCRDD), Longhua Hospital, Shanghai University of Traditional Chinese Medicine, 200032, Shanghai, China.
Wenjun ZhouInstitute of Digestive Diseases, China-Canada Center of Research for Digestive Diseases (ccCRDD), Longhua Hospital, Shanghai University of Traditional Chinese Medicine, 200032, Shanghai, China.
Jianping ZuoLaboratory of Immunology and Virology, Shanghai University of Traditional Chinese Medicine, 201203, Shanghai, China.
Zemin YaoDepartment of Biochemistry, Microbiology & Immunology, Ottawa Institute of Systems Biology, University of Ottawa, K1H 8M5, Ottawa, Canada.
Li ZhangInstitute of Digestive Diseases, China-Canada Center of Research for Digestive Diseases (ccCRDD), Longhua Hospital, Shanghai University of Traditional Chinese Medicine, 200032, Shanghai, China. zhangli.hl@163.com.
Guang JiInstitute of Digestive Diseases, China-Canada Center of Research for Digestive Diseases (ccCRDD), Longhua Hospital, Shanghai University of Traditional Chinese Medicine, 200032, Shanghai, China. jiliver@vip.sina.com.ORCID http://orcid.org/0000-0003-0842-3676
Shanghai University of Traditional Chinese Medicine · CNUniversity of Ottawa · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Berberine (BBR) is a widely used anti-diabetic agent, and liver glucokinase (GK) has been reported to be involved. However, the mechanisms of BBR in regulating GK are still unknown. Here, we found that BBR upregulated GK immunofluorescence expression in AML12 cells cultured in high glucose and increased glycogen content simultaneously. BBR improved hyperglycemia in db/db mice, and increased liver glucose-6-phosphate/glucose-1-phosphate (G-6-P/G-1-P) was found by analyzing metabolites (serum, liver, and feces) based on gas chromatography-mass spectrometry (GC-MS) metabolomics. Pharmacokinetics-pharmacodynamics (PK-PD) assessment revealed enriched BBR distribution in the liver, and liver G-6-P had the same trend as the concentration-time curve of BBR. G-6-P is solely catalyzed by GK, and GK activity and expression showed a positive correlation with liver BBR levels. In db/db mice, BBR also upregulated GK in liver fractions (cytoplasm and nucleus) and liver glycogen content. GK functionally worked by dissociating from GK regulatory protein (GKRP), and although GKRP expression was not affected, we found a decreased ratio of GK binding with GKRP in BBR treated db/db mice. In conclusion, our study suggests the dissociation of GK from GKRP as the potential mechanism for liver GK increase upon BBR treatment, which contributes to the anti-diabetic effect of BBR.

Indexed as

AnimalsBerberineBlood GlucoseDiabetes Mellitus, Type 2GlucokinaseGlucoseHepatocytesHumansHyperglycemiaHypoglycemic AgentsInsulinLiverLiver GlycogenMaleMiceMice, Inbred NODBerberineBlood GlucoseGlucokinaseGlucoseHypoglycemic AgentsInsulinLiver Glycogen

Identifiers

PMID31142783
PMCPMC6541623
OpenAlexW2947875000

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.