Resistance Exercise Improves Glycolipid Metabolism and Mitochondrial Biogenesis in Skeletal Muscle of T2DM Mice via miR-30d-5p/SIRT1/PGC-1α Axis
Open accessAbstract
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.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Resistance exercise improves glycolipid metabolism and mitochondrial biogenesis through pathways such as the miR-30d-5p/SIRT1/PGC-1α axis, as evidenced by studies in type 2 diabetes mellitus (T2DM) models.
“At the molecular level, resistance exercise improves glycolipid metabolism and mitochondrial biogenesis through pathways such as the miR-30d-5p/SIRT1/PGC-1α axis, as evidenced by studies in type 2 diabetes mellitus (T2DM) models.”
From Beyond Calories: Individual Metabolic and Hormonal Adaptations Driving Variability in Weight Management—A State-of-the-Art Narrative Review (2024) · cites this paper as [104]
This increase in muscle mass counteracts metabolic adaptations, such as the reduction in energy expenditure often observed during caloric restriction, thereby enhancing the sustainability of weight loss efforts.
“This increase in muscle mass also counteracts metabolic adaptations, such as the reduction in energy expenditure often observed during caloric restriction, thereby enhancing the sustainability of weight loss efforts.”
From Beyond Calories: Individual Metabolic and Hormonal Adaptations Driving Variability in Weight Management—A State-of-the-Art Narrative Review (2024) · cites this paper as [104]
By increasing lean muscle mass, strength training elevates the RMR, leading to greater caloric expenditure even at rest.
“By increasing lean muscle mass, strength training elevates the RMR, leading to greater caloric expenditure even at rest.”
From Beyond Calories: Individual Metabolic and Hormonal Adaptations Driving Variability in Weight Management—A State-of-the-Art Narrative Review (2024) · cites this paper as [104]
Lifang Zheng et al. demonstrated that resistance exercise significantly improves glucose homeostasis, insulin signaling, and mitochondrial function in T2DM mice by downregulating miR-30d-5p, which targets SIRT1 and impacts PGC-1α expression.
“Lifang Zheng et al. demonstrated that resistance exercise significantly improves glucose homeostasis, insulin signaling, and mitochondrial function in T2DM mice by downregulating miR-30d-5p, which targets SIRT1 and impacts PGC-1α expression.”
From Beyond Calories: Individual Metabolic and Hormonal Adaptations Driving Variability in Weight Management—A State-of-the-Art Narrative Review (2024) · cites this paper as [104]
These findings underscore the role of strength training in reducing lipid accumulation, enhancing fatty acid oxidation, and regulating key molecular pathways that mitigate insulin resistance.
“These findings underscore the role of strength training in not only reducing lipid accumulation and enhancing fatty acid oxidation but also in regulating key molecular pathways that mitigate insulin resistance [104].”
From Beyond Calories: Individual Metabolic and Hormonal Adaptations Driving Variability in Weight Management—A State-of-the-Art Narrative Review (2024) · cites this paper as [104]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 56 · Cited by 25
Research works printed but not linked: 1
- [1]IDF Diabetes Atlas Available online: https://diabetesatlas.org/atlas/ninth-edition/ (accessed on 1 October 2024)
- Authors
- Zheng, L., Rao, Z., Wu, J., Ma, X., Jiang, Z., & Xiao, W.
- Affiliations
- Shanghai University (CN)
- Shanghai Normal University (CN)
- Shanghai University of Sport (CN)
- Corresponding author
- Xiao, Weihua
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2024-11-19
- Volume
- 25
- Issue
- 22
- Pages
- 12416
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC11595072
- OpenAlex
- W4404502183
- Cited by
- 25
- References
- 56
- Citations by year
- 2026: 11 · 2025: 13 · 2024: 1
- FWCI
- 3.40
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (32371185, 32400956, 23010504200, 20SG50, 2020125, 2022KF001, 11DZ2261100)
- Shanghai Science and Technology Plan Project (32371185, 32400956, 23010504200, 20SG50, 2020125, 2022KF001, 11DZ2261100)
- “Shuguang Program” funded by Shanghai Education Development Foundation and Shanghai Municipale Education Commission (32371185, 32400956, 23010504200, 20SG50, 2020125, 2022KF001, 11DZ2261100)
- Shanghai Talent Development Fund (32371185, 32400956, 23010504200, 20SG50, 2020125, 2022KF001, 11DZ2261100)
- Key Lab of Exercise and Health Sciences of Ministry of Education (Shanghai University of Sport) (32371185, 32400956, 23010504200, 20SG50, 2020125, 2022KF001, 11DZ2261100)
- Shanghai Key Lab of Human Performance (Shanghai University of Sport) (32371185, 32400956, 23010504200, 20SG50, 2020125, 2022KF001, 11DZ2261100)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Keywords
- resistance training, type 2 diabetes, miR-30d-5p, SIRT1, PGC-1α, mitochondrial biogenesis, mitochondrial dynamics, skeletal muscle, glycolipid metabolism, insulin signaling, glucose uptake, lipid accumulation, microRNA therapeutic target
- MeSH terms
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Animals, Organelle Biogenesis, Diabetes Mellitus, Type 2, Glycolipids, Insulin Resistance, Male, Mice, Inbred C57BL, Physical Conditioning, Animal, Signal Transduction, Muscle, Skeletal, MicroRNAs, Lipid Metabolism, Mice, Resistance Training, Sirtuin 1
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
