ArticleEMBO reports2021
miR-183 and miR-96 orchestrate both glucose and fat utilization in skeletal muscle.
Article in EMBO reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Serum-Derived Extracellular Vesicles as Biological Indicator of Mobility Resilience in Older Adults.Aging cell · 2026Article
- CircDCAF6 regulates the miR-196a/IGF2BP3 axis to promote proliferation and inhibit apoptosis in bovine myoblasts.Protoplasma · 2026Article
- Epinephrine promotes breast cancer metastasis through a ubiquitin-specific peptidase 22-mediated lipolysis circuit.Science advances · 2024Article
- Emerging roles of noncoding RNAs in human cancers.Discover oncology · 2023Review
- MicroRNA-200c-5p Regulates Migration and Differentiation of Myoblasts via TargetingInternational journal of molecular sciences · 2023Article
- miR-183/96/182 Cluster Regulates the Development of Bovine Myoblasts through TargetingAnimals : an open access journal from MDPI · 2022Article
- G6PD Deficiency Is Crucial for Insulin Signaling Activation in Skeletal Muscle.International journal of molecular sciences · 2022Article
- miR-183 and miR-96 orchestrate both glucose and fat utilization in skeletal muscle.EMBO reports · 2021Article
- Comprehensive Analysis of mRNA, lncRNA, circRNA, and miRNA Expression Profiles and Their ceRNA Networks in theFrontiers in genetics · 2021Article
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our knowledge of the coordination of fuel usage in skeletal muscle is incomplete. Whether and how microRNAs are involved in the substrate selection for oxidation is largely unknown. Here we show that mice lacking miR-183 and miR-96 have enhanced muscle oxidative phenotype and altered glucose/lipid homeostasis. Moreover, loss of miR-183 and miR-96 results in a shift in substrate utilization toward fat relative to carbohydrates in mice. Mechanistically, loss of miR-183 and miR-96 suppresses glucose utilization in skeletal muscle by increasing PDHA1 phosphorylation via targeting FoxO1 and PDK4. On the other hand, loss of miR-183 and miR-96 promotes fat usage in skeletal muscle by enhancing intramuscular lipolysis via targeting FoxO1 and ATGL. Thus, our study establishes miR-183 and miR-96 as master coordinators of fuel selection and metabolic homeostasis owing to their capability of modulating both glucose utilization and fat catabolism. Lastly, we show that loss of miR-183 and miR-96 can alleviate obesity and improve glucose metabolism in high-fat diet-induced mice, suggesting that miR-183 and miR-96 may serve as therapeutic targets for metabolic diseases.
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Registered trials
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.