Evidence map›Paper›PMID 40046742›Full record

ArticleFrontiers in pharmacology2025

Exploring the glucose-lowering and anti-inflammatory immune mechanism of artemether by AMPK/mTOR pathway and microbiome based on multi-omics.

Tao Jiang, Peipei Du, Dongxia Liu, Hetao Chen, Yujin Ma, Bin Hu, Jingna Li, Hongwei Jiang, Xuejiao Li

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 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

9 authors.

Tao Jiang *Department of Clinical Laboratory, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Peipei Du *Department of Clinical Laboratory, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Dongxia LiuDepartment of Clinical Laboratory, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Hetao ChenDepartment of Clinical Laboratory, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Yujin MaLuoyang Key Laboratory of Clinical Multiomics and Translational Medicine, Key Laboratory of Hereditary Rare Diseases of Health Commission of Henan Province, Henan Key Laboratory of Rare Diseases, Endocrinology and Metabolism Center, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Bin HuDepartment of Pharmacy, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Jingna LiDepartment of Pharmacy, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Hongwei JiangLuoyang Key Laboratory of Clinical Multiomics and Translational Medicine, Key Laboratory of Hereditary Rare Diseases of Health Commission of Henan Province, Henan Key Laboratory of Rare Diseases, Endocrinology and Metabolism Center, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Xuejiao LiLuoyang Key Laboratory of Clinical Multiomics and Translational Medicine, Key Laboratory of Hereditary Rare Diseases of Health Commission of Henan Province, Henan Key Laboratory of Rare Diseases, Endocrinology and Metabolism Center, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Diabetes mellitus (DM) is a metabolic disease with high morbidity, which significantly affects human life and health expenditures. Previous studies have demonstrated that artemether (ATM) has anti-diabetes and anti-inflammation activities, but its mechanism has not been fully elucidated. This research aimed to elucidate the impact of ATM on glucolipid metabolism in a type 2 diabetes mellitus (T2DM) model db/db mice and what kind of role the gut microbiota played, and explored the underlying mechanisms involved. Methods: C57BL/KsJ-db/db mice were treated with 80 and 160 mg/kg of ATM for 8 weeks, with metformin as a positive control. Results: ATM treatment (160 mg/kg) observably ameliorated insulin resistance (IR), hyperglycemia, hyperlipemia and pathological injury in the liver and pancreas. In addition, ATM significantly decreased the expression of TNF-α, IL-1β, IL-6, NF-κB and IL-17A, and significantly increased the level of IL-10 in diabetic mice. 16S rRNA sequencing and targeted GC-MS metabolomics result indicated that ATM restored gut microbiota dysbiosis based on increasing beneficial bacteria Conclusion: Taken together, ATM may modulate the composition of gut microbiota, increasing the abundance of

Indexed as

AMPK/mTOR pathwayartemethergut microbiotametabolomicsnetwork pharmacologyT2DM

Identifiers

PMID40046742
PMCPMC11879814

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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.