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MicroRNA-126b-5p Exacerbates Development of Adipose Tissue and Diet-Induced Obesity
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...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8508536/ https://www.ncbi.nlm.nih.gov/pubmed/34638602 http://dx.doi.org/10.3390/ijms221910261 |
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author | Shen, Linyuan He, Jin Zhao, Ye Niu, Lili Chen, Lei Tang, Guoqing Jiang, Yanzhi Hao, Xiaoxia Bai, Lin Li, Xuewei Zhang, Shunhua Zhu, Li |
author_facet | Shen, Linyuan He, Jin Zhao, Ye Niu, Lili Chen, Lei Tang, Guoqing Jiang, Yanzhi Hao, Xiaoxia Bai, Lin Li, Xuewei Zhang, Shunhua Zhu, Li |
author_sort | Shen, Linyuan |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-8508536 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-85085362021-10-13 MicroRNA-126b-5p Exacerbates Development of Adipose Tissue and Diet-Induced Obesity Shen, Linyuan He, Jin Zhao, Ye Niu, Lili Chen, Lei Tang, Guoqing Jiang, Yanzhi Hao, Xiaoxia Bai, Lin Li, Xuewei Zhang, Shunhua Zhu, Li Int J Mol Sci Article 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. MDPI 2021-09-23 /pmc/articles/PMC8508536/ /pubmed/34638602 http://dx.doi.org/10.3390/ijms221910261 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Shen, Linyuan He, Jin Zhao, Ye Niu, Lili Chen, Lei Tang, Guoqing Jiang, Yanzhi Hao, Xiaoxia Bai, Lin Li, Xuewei Zhang, Shunhua Zhu, Li MicroRNA-126b-5p Exacerbates Development of Adipose Tissue and Diet-Induced Obesity |
title | MicroRNA-126b-5p Exacerbates Development of Adipose Tissue and Diet-Induced Obesity |
title_full | MicroRNA-126b-5p Exacerbates Development of Adipose Tissue and Diet-Induced Obesity |
title_fullStr | MicroRNA-126b-5p Exacerbates Development of Adipose Tissue and Diet-Induced Obesity |
title_full_unstemmed | MicroRNA-126b-5p Exacerbates Development of Adipose Tissue and Diet-Induced Obesity |
title_short | MicroRNA-126b-5p Exacerbates Development of Adipose Tissue and Diet-Induced Obesity |
title_sort | microrna-126b-5p exacerbates development of adipose tissue and diet-induced obesity |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8508536/ https://www.ncbi.nlm.nih.gov/pubmed/34638602 http://dx.doi.org/10.3390/ijms221910261 |
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