Evidence map›Paper›PMID 35869471›Full record

ArticleBMC endocrine disorders2022

Metformin activates Wnt/β-catenin for the treatment of diabetic osteoporosis.

Xiaopeng Huang, Siyun Li, Wenjie Lu, Longjiang Xiong

Open access · goldFull text read
In one paragraph

Article in BMC endocrine disorders, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Review
  6. Article
  7. Wnt/β-Catenin Signaling in Diabetic Complications: Mechanisms and Therapeutic Potential.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Metformin and bone metabolism: unraveling their direct and indirect effects.Therapeutic advances in endocrinology and metabolism · 2025
    Review
  14. Review
  15. Osteoporosis in Adrenal Insufficiency: Could Metformin be Protective?Indian journal of clinical biochemistry : IJCB · 2025
    Review
  16. Article
  17. Article
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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

4 authors at 1 institution in 1 country.

Xiaopeng HuangDepartment of Orthopedics, Jiangxi Province Hospital of Integrated Chinese & Western Medicine, Nanchang, 330003, China.
Siyun LiDepartment of Orthopedics, Jiangxi Province Hospital of Integrated Chinese & Western Medicine, Nanchang, 330003, China.
Wenjie LuDepartment of Orthopedics, Jiangxi Province Hospital of Integrated Chinese & Western Medicine, Nanchang, 330003, China.
Longjiang XiongDepartment of Orthopedics, Jiangxi Province Hospital of Integrated Chinese & Western Medicine, Nanchang, 330003, China. xlj95196@163.com.
Integrated Chinese Medicine (China) · CN

Funding

Science and Technology Plan of Health Commission of Jiangxi Province (NO.SKJP220200605)
6 · The paper itself

Abstract

backgroundWith the deepening of social aging, the incidence rate of osteoporosis and diabetes continues to rise. More and more clinical studies show that diabetes is highly correlated with osteoporosis. Diabetes osteoporosis is considered as a metabolic bone disease of diabetes patients. This study aims to explore the role and mechanism of metformin (Met) in diabetic osteoporosis.

methodsMouse MC3T3-E1 cells were treated with Met (0.5 mM) and exposed to high glucose (HG, 35 mM). The cells were cultured in an osteogenic medium for osteogenic differentiation, and the cell proliferation ability was determined using Cell Counting Kit-8; Alkaline phosphatase (ALP) activity detection and alizarin red staining were utilized to evaluate the effect of Met on MC3T3-E1 osteogenic differentiation. Western blot was used to detect the expressions of osteogenesis-related proteins (Runx2 and OCN) as well as Wnt/β-catenin signaling pathway-related proteins in MC3T3-E1 cells.

resultsHG inhibited proliferation and calcification of MC3T3-E1 cells, down-regulated ALP activity, and the expression of Runx2 and OCN in MC3T3-E1 cells. Meanwhile, the activity of the Wnt/β-catenin signaling pathway was inhibited. Met treatment was found to significantly stimulate the proliferation and calcification of MC3T3-E1 cells under HG conditions, as well as increase the ALP activity and the protein expression level of Runx2 and OCN in the cells. As a result, osteogenic differentiation was promoted and osteoporosis was alleviated. Apart from this, Met also increased the protein expression level of Wnt1, β-catenin, and C-myc to activate the Wnt/β-catenin signaling pathway.

conclusionMet can stimulate the proliferation and osteogenic differentiation of MC3T3-E1 cells under HG conditions. Met may also treat diabetic osteoporosis through Wnt/β-catenin activation.

Indexed as

Diabetes MellitusMetforminOsteoporosisAnimalsbeta CateninCore Binding Factor Alpha 1 SubunitMiceOsteoblastsOsteogenesisWnt Proteinsbeta CateninCore Binding Factor Alpha 1 SubunitCTNNB1 protein, mouseMetforminWnt ProteinsDiabetes mellitus (DM)MetforminOsteoporosisWnt/β-catenin

Identifiers

PMID35869471
PMCPMC9306077
OpenAlexW4286471150

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Registered trials

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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.