MiR-125b-2 knockout increases high-fat diet-induced fat accumulation and insulin resistance

Abstract Obese individuals are more susceptible to comorbidities than individuals of healthy weight, including cardiovascular disease and metabolic disorders. MicroRNAs are a class of small and noncoding RNAs that are implicated in the regulation of chronic human diseases. We previously reported tha...

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Autores principales:	Li-Min Wei, Rui-Ping Sun, Tao Dong, Jie Liu, Ting Chen, Bin Zeng, Jia-Han Wu, Jun-yi Luo, Jia-Jie Sun, Qian-Yun Xi, Yong-Liang Zhang
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2020
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/049c57d96a494627bab4056c0d54b858
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spelling	oai:doaj.org-article:049c57d96a494627bab4056c0d54b8582021-12-02T13:34:10ZMiR-125b-2 knockout increases high-fat diet-induced fat accumulation and insulin resistance10.1038/s41598-020-77714-72045-2322https://doaj.org/article/049c57d96a494627bab4056c0d54b8582020-12-01T00:00:00Zhttps://doi.org/10.1038/s41598-020-77714-7https://doaj.org/toc/2045-2322Abstract Obese individuals are more susceptible to comorbidities than individuals of healthy weight, including cardiovascular disease and metabolic disorders. MicroRNAs are a class of small and noncoding RNAs that are implicated in the regulation of chronic human diseases. We previously reported that miR-125b plays a critical role in adipogenesis in vitro. However, the involvement of miR-125b-2 in fat metabolism in vivo remains unknown. In the present study, miR-125b-2 knockout mice were generated using CRISPR/CAS9 technology, resulting in mice with a 7 bp deletion in the seed sequence of miR-125b-2. MiR-125b-2 knockout increased the weight of liver tissue, epididymal white fat and inguinal white fat. MiR-125b-2 knockout also increased adipocyte volume in HFD-induced obese mice, while there were no significant differences in body weight and feed intake versus mice fed a normal diet. Additionally, qRT-PCR and western blot analysis revealed that the expression of the miR-125b-2 target gene SCD-1 and fat synthesis-associated genes, such as PPARγ and C/EBPα, were significantly up-regulated in miR-125b-2KO mice (P < 0.05). Moreover, miR-125b-2KO altered HFD-induced changes in glucose tolerance and insulin resistance. In conclusion, we show that miR-125b-2 is a novel potential target for regulating fat accumulation, and also a candidate target to develop novel treatment strategies for obesity and diabetes.Li-Min WeiRui-Ping SunTao DongJie LiuTing ChenBin ZengJia-Han WuJun-yi LuoJia-Jie SunQian-Yun XiYong-Liang ZhangNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 10, Iss 1, Pp 1-10 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Li-Min Wei Rui-Ping Sun Tao Dong Jie Liu Ting Chen Bin Zeng Jia-Han Wu Jun-yi Luo Jia-Jie Sun Qian-Yun Xi Yong-Liang Zhang MiR-125b-2 knockout increases high-fat diet-induced fat accumulation and insulin resistance
description	Abstract Obese individuals are more susceptible to comorbidities than individuals of healthy weight, including cardiovascular disease and metabolic disorders. MicroRNAs are a class of small and noncoding RNAs that are implicated in the regulation of chronic human diseases. We previously reported that miR-125b plays a critical role in adipogenesis in vitro. However, the involvement of miR-125b-2 in fat metabolism in vivo remains unknown. In the present study, miR-125b-2 knockout mice were generated using CRISPR/CAS9 technology, resulting in mice with a 7 bp deletion in the seed sequence of miR-125b-2. MiR-125b-2 knockout increased the weight of liver tissue, epididymal white fat and inguinal white fat. MiR-125b-2 knockout also increased adipocyte volume in HFD-induced obese mice, while there were no significant differences in body weight and feed intake versus mice fed a normal diet. Additionally, qRT-PCR and western blot analysis revealed that the expression of the miR-125b-2 target gene SCD-1 and fat synthesis-associated genes, such as PPARγ and C/EBPα, were significantly up-regulated in miR-125b-2KO mice (P < 0.05). Moreover, miR-125b-2KO altered HFD-induced changes in glucose tolerance and insulin resistance. In conclusion, we show that miR-125b-2 is a novel potential target for regulating fat accumulation, and also a candidate target to develop novel treatment strategies for obesity and diabetes.
format	article
author	Li-Min Wei Rui-Ping Sun Tao Dong Jie Liu Ting Chen Bin Zeng Jia-Han Wu Jun-yi Luo Jia-Jie Sun Qian-Yun Xi Yong-Liang Zhang
author_facet	Li-Min Wei Rui-Ping Sun Tao Dong Jie Liu Ting Chen Bin Zeng Jia-Han Wu Jun-yi Luo Jia-Jie Sun Qian-Yun Xi Yong-Liang Zhang
author_sort	Li-Min Wei
title	MiR-125b-2 knockout increases high-fat diet-induced fat accumulation and insulin resistance
title_short	MiR-125b-2 knockout increases high-fat diet-induced fat accumulation and insulin resistance
title_full	MiR-125b-2 knockout increases high-fat diet-induced fat accumulation and insulin resistance
title_fullStr	MiR-125b-2 knockout increases high-fat diet-induced fat accumulation and insulin resistance
title_full_unstemmed	MiR-125b-2 knockout increases high-fat diet-induced fat accumulation and insulin resistance
title_sort	mir-125b-2 knockout increases high-fat diet-induced fat accumulation and insulin resistance
publisher	Nature Portfolio
publishDate	2020
url	https://doaj.org/article/049c57d96a494627bab4056c0d54b858
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MiR-125b-2 knockout increases high-fat diet-induced fat accumulation and insulin resistance

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