ArticleInternational journal of molecular sciences2021
MicroRNA-126b-5p Exacerbates Development of Adipose Tissue and Diet-Induced Obesity.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Cooked meat-derived extracellular vesicles ssc-miR-1 induces metabolic disorders in the mice liver via PI3k/AKT pathway.NPJ science of food · 2026Article
- Therapeutic Applications of Poly-miRNAs and miRNA Sponges.International journal of molecular sciences · 2025Review
- Compound probiotics promote the growth of piglets through activating the JAK2/STAT5 signaling pathway.Frontiers in microbiology · 2025Article
- Childhood obesity, metabolic syndrome, and oxidative stress: microRNAs go on stage.Reviews in endocrine & metabolic disorders · 2023Review
- Effect of ACADL on the differentiation of goat subcutaneous adipocyte.Animal bioscience · 2023Article
- Cooked pork-derived exosome nanovesicles mediate metabolic disorder-microRNA could be the culprit.Journal of nanobiotechnology · 2023Article
- LncGenes · 2023Article
- Differential Expression Analysis of tRNA-Derived Small RNAs from Subcutaneous Adipose Tissue of Obese and Lean Pigs.Animals : an open access journal from MDPI · 2022Article
- Physical Activity Rewires the Human Brain against Neurodegeneration.International journal of molecular sciences · 2022Article
- Establishment and validation of a cholesterol metabolism-related prognostic signature for hepatocellular carcinoma.Computational and structural biotechnology journal · 2022Article
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Authors and funding
12 authors.
Funding
Abstract
Obesity has become a worldwide epidemic, caused by many factors such as genetic regulatory elements, unhealthy diet, and lack of exercise. MicroRNAs (miRNAs) are non-coding single-stranded RNA classes, which are about 22 nucleotides in length and highly conserved among species. In the last decade, a series of miRNAs were identified as therapeutic targets for obesity. In the present study, we found that miR-126b-5p was associated with adipogenesis. miR-126b-5p overexpression promoted the proliferation of 3T3-L1 preadipocytes by upregulating the expression of proliferation-related genes and downregulating the expression of apoptosis-related genes; the inhibition of miR-126b-5p gave rise to opposite results. Similarly, miR-126b-5p overexpression could promote the differentiation of 3T3-L1 preadipocytes by increasing the expression of lipid deposition genes and triglyceride (TG) and total cholesterol (TC) levels. Moreover, luciferase reporter assay demonstrated that adiponectin receptor 2 (Adipor2) and acyl-CoA dehydrogenase, long chain (ACADL) were the direct target genes of miR-126b-5p. Moreover, overexpression of miR-126b-5p could exacerbate the clinical symptoms of obesity when mice were induced by a high-fat diet, including increased adipose tissue weight, adipocyte volume, and insulin resistance. Interestingly, overexpression of miR-126b-5p in preadipocytes and mice could significantly increase total fatty acid content and change the fatty acid composition of adipose tissue. Taken together, the present study showed that miR-126b-5p promotes lipid deposition in vivo and in vitro, indicating that miR-126b-5p is a potential target for treating obesity.
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Registered trials
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