Evidence map›Paper›PMID 33062529›Full record

ReviewCureus2020

The Future of Metformin in the Prevention of Diabetes-Related Osteoporosis.

Myat Aung, Saba Amin, Azouba Gulraiz, Fenil R Gandhi, Julio A Pena Escobar, Bilal Haider Malik

Abstract readReview
In one paragraph

Review in Cureus, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
–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

15 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  9. Article
  10. Exogenous melatonin prevents type 1 diabetes mellitus-induced bone loss, probably by inhibiting senescence.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2022
    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

6 authors.

Myat AungMedicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Saba AminMedicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Azouba GulraizMedicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Fenil R GandhiMedicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Julio A Pena EscobarMedicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Bilal Haider MalikMedicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As a worldwide aging population is on the rise, osteoporosis (OS) is becoming a global health burden. Therefore, many researchers and health authorities are looking into the potential prevention and treatment of OS. Although previously regarded as two separate pathological processes, diabetes (DM) and OS are now regarded as two conditions that can occur together. It is now believed that OS can develop as a complication of DM. This relationship is further evidenced through a reduction in bone mineral density in type-1 diabetes with a resulting increased risk of fracture. Although bone mineral density in type-2 diabetes mellitus is normal or increased, there is also increased fragility due to decreased bone quality. These abnormal bone qualities tend to occur through the production of reduced bone microvasculature and advanced glycation end product, AGE. Interestingly, one of the most common treatments for DM, metformin (MF), shows a promising result on the protection of diabetes and non-diabetes related bone turnover. It is believed that MF modulates its effect through the adenosine monophosphate-activated protein kinase (AMPK) pathway. Recent data regarded AMPK as a vital mediator of homeostasis. It is involved not only in glucose metabolism but also in osteogenesis. AMPK can directly influence the production of mature and good quality bone by decreasing osteoclasts, increasing osteoblast formation, and enhancing bone mineral deposition. As an activator of AMPK, MF also upregulates osteogenesis. Furthermore, MF can influence osteogenesis through a non-AMPK pathway, such as the fructose 1-6 phosphatase pathway, by reducing glucose levels. While already recognized as a safe and effective treatment for DM, this article discusses whether MF can be used for the prevention and treatment of OS.

Indexed as

ampkbone disorderdiabetesmetforminosteogenesisosteoporosis

Identifiers

PMID33062529
PMCPMC7550241

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.