Evidence map›Paper›PMID 39596482›Full record

ArticleInternational journal of molecular sciences2024

Resistance Exercise Improves Glycolipid Metabolism and Mitochondrial Biogenesis in Skeletal Muscle of T2DM Mice via miR-30d-5p/SIRT1/PGC-1α Axis.

Lifang Zheng, Zhijian Rao, Jiabin Wu, Xiaojie Ma, Ziming Jiang, Weihua Xiao

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

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  17. Effects of atmospherically relevant PMFrontiers in public health · 2025
    Review
  18. Review
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.

Lifang ZhengCollege of Physical Education, Shanghai University, Shanghai 200444, China.
Zhijian RaoCollege of Physical Education, Shanghai Normal University, Shanghai 200234, China.
Jiabin WuShanghai Key Laboratory of Human Performance, Shanghai University of Sport, Shanghai 200438, China.
Xiaojie MaCollege of Physical Education, Shanghai University, Shanghai 200444, China.
Ziming JiangCollege of Physical Education, Shanghai University, Shanghai 200444, China.
Weihua XiaoShanghai Key Laboratory of Human Performance, Shanghai University of Sport, Shanghai 200438, China.

Funding

National Natural Science Foundation of China 32371185the Key Lab of Exercise and Health Sciences of Ministry of Education (Shanghai University of Sport) 2022KF001the National Natural Science Foundation of China 32400956the Shanghai Key Lab of Human Performance (Shanghai University of Sport) NO. 11DZ2261100the Shanghai Science and Technology Plan Project 23010504200the Shanghai Talent Development Fund 2020125the "Shuguang Program funded by Shanghai Education Development Foundation and Shanghai Municipale Education Commission 20SG50
6 · The paper itself

Abstract

Exercise is a recognized non-pharmacological treatment for improving glucose homeostasis in type 2 diabetes (T2DM), with resistance exercise (RE) showing promising results. However, the mechanism of RE improving T2DM has not been clarified. This study aims to investigate the effects of RE on glucose and lipid metabolism, insulin signaling, and mitochondrial function in T2DM mice, with a focus on the regulatory role of miR-30d-5p. Our results confirmed that RE significantly improved fasting blood glucose, IPGTT, and ITT in T2DM mice. Enhanced expression of IRS-1, p-PI3K, and p-Akt indicated improved insulin signaling. RE improved glycolipid metabolism, as well as mitochondrial biogenesis and dynamics in skeletal muscle of T2DM mice. We also found that miR-30d-5p was upregulated in T2DM, and was downregulated after RE. Additionally, in vitro, over-expression of miR-30d-5p significantly increased lipid deposition, and reduced glucose uptake and mitochondrial biogenesis. These observations were reversed after transfection with the miR-30d-5p inhibitor. Mechanistically, miR-30d-5p regulates glycolipid metabolism in skeletal muscle by directly targeting SIRT1, which affects the expression of PGC-1α, thereby influencing mitochondrial function and glycolipid metabolism. Taken together, RE effectively improves glucose and lipid metabolism and mitochondrial function in T2DM mice, partly through regulating the miR-30d-5p/SIRT1/PGC-1α axis. miR-30d-5p could serve as a potential therapeutic target for T2DM management.

Indexed as

Diabetes Mellitus, Type 2GlycolipidsMicroRNAsMuscle, SkeletalOrganelle BiogenesisPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhysical Conditioning, AnimalSirtuin 1AnimalsInsulin ResistanceLipid MetabolismMaleMiceMice, Inbred C57BLResistance TrainingSignal TransductionGlycolipidsMicroRNAsMirn30d microRNA, mousePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseSirt1 protein, mouseSirtuin 1insulin resistancemiRNAsresistance exerciseskeletal muscleT2DM

Identifiers

PMID39596482
PMCPMC11595072

What Socratic holds

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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.