Evidence map›Paper›PMID 35802043›Full record

ArticleDiabetes2022

Exercise-Linked Skeletal Irisin Ameliorates Diabetes-Associated Osteoporosis by Inhibiting the Oxidative Damage-Dependent miR-150-FNDC5/Pyroptosis Axis.

Jyotirmaya Behera, Jessica Ison, Michael J Voor, Neetu Tyagi

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Diabetes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 2 pooled it
10.4field-weighted citation impact, top 1% 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

68 citing papers in PubMed, 2 syntheses or guidelines pooled it, 92 citations in OpenAlex.

  1. Protective role of irisin on bone in osteoporosis: a systematic review of rodent studies.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2025
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  4. Glucose metabolism in osteoporosis: A potential therapeutic target (Review).International journal of molecular medicine · 2026
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8 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Jyotirmaya BeheraBone Biology Laboratory, Department of Physiology, School of Medicine, University of Louisville, Louisville, KY.
Jessica IsonBone Biology Laboratory, Department of Physiology, School of Medicine, University of Louisville, Louisville, KY.
Michael J VoorDepartments of Orthopaedic Surgery and Bioengineering, School of Medicine, University of Louisville, Louisville, KY.
Neetu TyagiBone Biology Laboratory, Department of Physiology, School of Medicine, University of Louisville, Louisville, KY.ORCID 0000-0002-1789-0754
University of Louisville · US

Funding

Mitigating mitochondrial epigenetics in bone remodeling by hydrogen sulfideR01AR067667 · NIAMS · UNIVERSITY OF LOUISVILLE · PI TYAGI, NEETU, TYAGI, SURESH C. · 2015 to 2019
$2.5M
NIAMS NIH HHS R01 AR067667
6 · The paper itself

Abstract

Recent evidence suggests that physical exercise (EX) promotes skeletal development. However, the impact of EX on the progression of bone loss and deterioration of mechanical strength in mice with type 2 diabetic mellitus (T2DM) remains unexplored. In the current study, we investigated the effect of EX on bone mass and mechanical quality using a diabetic mouse model. The T2DM mouse model was established with a high-fat diet with two streptozotocin injections (50 mg/kg/body wt) in C57BL/6 female mice. The diabetic mice underwent treadmill exercises (5 days/week at 7-11 m/min for 60 min/day) for 8 weeks. The data showed that diabetes upregulated miR-150 expression through oxidative stress and suppressed FNDC5/Irisin by binding to its 3'-untranslated region. The decreased level of irisin further triggers the pyroptosis response in diabetic bone tissue. EX or N-acetyl cysteine or anti-miRNA-150 transfection in T2DM mice restored FNDC5/Irisin expression and bone formation. Furthermore, EX or recombinant irisin administration prevented T2DM-Induced hyperglycemia and improved glucose intolerance in diabetic mice. Furthermore, osteoblastic knockdown of Nlrp3 silencing (si-Nlrp3) or pyroptosis inhibitor (Ac-YVADCMK [AYC]) treatment restores bone mineralization in diabetic mice. Micro-computed tomography scans and mechanical testing revealed that trabecular bone microarchitecture and bone mechanical properties were improved after EX in diabetic mice. Irisin, either induced by skeleton or daily EX or directly administered, prevents bone loss by mitigating inflammasome-associated pyroptosis signaling in diabetic mice. This study demonstrates that EX-induced skeletal irisin ameliorates diabetes-associated glucose intolerance and bone loss and possibly provides a mechanism of its effects on metabolic osteoporosis.

Indexed as

Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2FibronectinsGlucose IntoleranceOsteoporosisAnimalsFemaleMiceMice, Inbred C57BLMicroRNAsMuscle, SkeletalNLR Family, Pyrin Domain-Containing 3 ProteinOxidative StressPyroptosisX-Ray MicrotomographyFibronectinsFNDC5 protein, mouseMicroRNAsMirn150 microRNA, mouseNLR Family, Pyrin Domain-Containing 3 Protein

Identifiers

PMID35802043
PMCPMC9750954
OpenAlexW4284975083

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.