ArticleMolecular and cellular biochemistry2020
LncRNA TUG1 reduces inflammation and enhances insulin sensitivity in white adipose tissue by regulating miR-204/SIRT1 axis in obesity mice.
Article in Molecular and cellular biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- Epigenetic Regulation of Sebaceous and Meibomian Glands: From Development to Disease.Biomedicines · 2026Review
- The Impact of Non-Coding RNA on Inflammation and Airway Remodeling in Asthma Related to Obesity: State-of-the-Art and Therapeutic Perspectives.Journal of clinical medicine · 2025Review
- Deciphering the role ofWorld journal of hepatology · 2025Review
- Obesity-induced adipocytes promote diabetes mellitus by regulating β islet cell function through exosome miR-138-5p.Scientific reports · 2025Article
- lncRNA TUG1 transcript levels and psychological disorders: insights into interplay of glycemic index and glycemic load.BMC medical genomics · 2024Article
- The transcript level of long non-coding RNAs; MALAT1 and TUG1, and the association with metabolic syndrome-related parameters in women with overweight and obesity.Journal of diabetes and metabolic disorders · 2024Article
- The interaction between MALAT1 and TUG1 with dietary fatty acid quality indices on visceral adiposity index and body adiposity index.Scientific reports · 2024Article
- The role of lncRNAs/miRNAs/Sirt1 axis in myocardial and cerebral injury.Cell cycle (Georgetown, Tex.) · 2023Review
- Long Noncoding RNAs in the Pathogenesis of Insulin Resistance.International journal of molecular sciences · 2022Review
- Construction and Comprehensive Analysis of miRNAs and Target mRNAs inLife (Basel, Switzerland) · 2022Article
- LncRNA TUG regulates osteogenic differentiation of bone marrow mesenchymal stem cells via miRNA-204/SIRT 1.Journal of musculoskeletal & neuronal interactions · 2022Article
- Review
- Review
- LncRNA Tug1 maintains blood-testis barrier integrity by modulating Ccl2 expression in high-fat diet mice.Cellular and molecular life sciences : CMLS · 2022Article
- Identification and analysis of lncRNA, miRNA and mRNA related to subcutaneous and intramuscular fat in Laiwu pigs.Frontiers in endocrinology · 2022Article
- Long non-coding RNAs in metabolic disorders: pathogenetic relevance and potential biomarkers and therapeutic targets.Journal of endocrinological investigation · 2021Review
- The PPARα and PPARγ Epigenetic Landscape in Cancer and Immune and Metabolic Disorders.International journal of molecular sciences · 2021Review
- Review
- Visceral Adipose Tissue of Prediabetic and Diabetic Females Shares a Set of Similarly Upregulated microRNAs Functionally Annotated to Inflammation, Oxidative Stress and Insulin Signaling.Antioxidants (Basel, Switzerland) · 2021Article
- Up-regulation of TUG1 can regulate miR-494/PDK4 axis to inhibit LPS-induced acute lung injury caused by sepsis.American journal of translational research · 2021Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prevalence of obesity becomes an important health issue worldwide, but the management of obesity remains unsatisfied. This study aimed to explore the mechanism of long non-coding RNA TUG/miR-204/SIRT1 axis, which was involved in the pathogenesis of obesity. Obesity mouse model was induced by high-fat diet and treated with taurine upregulated gene1 (TUG1) virus via tail intravenous injection. Then, body weight, serum glucose, insulin tolerance, testicular fat weight were detected, as well as the expression of TUG1, microRNA-204 (miR-204), sirtuin1 (SIRT1), and inflammation and fatty accumulation associated proteins and cytokines. Regulatory relationship between TUG1/SIRT1 and miR-204 was confirmed by dual-luciferase reporter activity assay. A high-glucose-induced 3T3-L1 cell model was also constructed to explore the regulatory mechanism of TUG/miR-204/SIRT1 axis in the pathogenesis of obesity at cell level after altering the expression of TUG1, miR-204, and SIRT1. Overexpression of TUG1 could significantly attenuate the weight, serum glucose, glucose, insulin tolerance, fatty accumulation, and inflammation in obesity mice, as well as the elevation of miR-204, but increase the expression of SIRT1, phosphorylated AKT (p-AKT), glucose transporter4 (GLUT4), and peroxisome proliferator activated receptorγ (PPARγ). Both TUG1 and SIRT1 were targets of miR-204 and could be negatively regulated by miR-204. Overexpression of TUG1 could suppress the inflammation in adipocytes via downregulating miR-204 and promote GLUT4/PPARγ/AKT pathway high-glucose-induced inflammation in 3T3-L1 cells. miR-204 inhibitors could also suppress high-glucose-induced inflammation in 3T3-L1 cells via promoting SIRT1/ GLUT4/PPARγ/AKT pathway. LncRNA TUG1 could negatively regulate miR-204 to alleviate inflammation and insulin tolerance via promoting SIRT1/GLUT4/PPARγ/AKT pathway.
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