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Isolation and Differentiation of Adipose-Derived Stem Cells from Porcine Subcutaneous Adipose Tissues
Published on: March 31, 2016
mRNA m⁶A methylation downregulates adipogenesis in porcine adipocytes
Xinxia Wang1, Linna Zhu1, Jingqing Chen1
1College of Animal Sciences, Zhejiang University, No. 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China; Key Laboratory of Animal Nutrition & Feed Sciences, Ministry of Agriculture, No. 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China; Zhejiang Provincial Laboratory of Feed and Animal Nutrition, No. 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China.
Abstract:
Fat Mass and Obesity-associated protein (FTO), associated with obesity, is proved to demethylate N6-methyladenosine (m(6)A), which raises questions regarding whether m(6)A plays vital roles in adipogenesis. To prove this, overexpression and knockdown of FTO and METTL3, as well as the chemical treatment in procine adipocytes were conducted. The results showed FTO negatively regulated m(6)A levels and positively regulated adipogenesis, while METTL3 positively correlated with m(6)A levels and negatively with adipogenesis. To remove the potential effect of FTO and METTL3 gene, chemical reagents of methylation inhibitor cycloleucine and methyl donor betaine were used to test the regulation effect of m(6)A on adipogenesis. The results showed the inverse effect of m(6)A on lipid accumulation in porcine adipocytes. These findings provide compelling evidence that m(6)A plays a critical role in the regulation of adipogenesis.
Insights
The study reveals that N6-methyladenosine (m(6)A) plays a crucial role in fat cell development (adipogenesis). Modulating m(6)A levels impacts fat accumulation, offering insights into obesity regulation.
Area of Science:
- Molecular Biology
- Epigenetics
- Cell Biology
Background:
- The Fat Mass and Obesity-associated protein (FTO) is linked to obesity and demethylates N6-methyladenosine (m(6)A).
- The precise role of m(6)A in adipogenesis remains unclear, prompting further investigation.
Purpose of the Study:
- To elucidate the role of m(6)A in regulating adipogenesis.
- To investigate the opposing effects of FTO and METTL3 on m(6)A levels and adipogenesis.
Main Methods:
- Overexpression and knockdown of FTO and METTL3 in porcine adipocytes.
- Chemical treatment using methylation inhibitor cycloleucine and methyl donor betaine.
- Assessment of m(6)A levels and lipid accumulation.
Main Results:
- FTO negatively regulated m(6)A levels and promoted adipogenesis.
- METTL3 positively correlated with m(6)A levels and inhibited adipogenesis.
- m(6)A demonstrated an inverse effect on lipid accumulation in porcine adipocytes.
Conclusions:
- m(6)A is a critical regulator of adipogenesis.
- FTO and METTL3 have opposing roles in m(6)A-mediated adipogenesis.
- Findings provide a basis for understanding obesity through epigenetic mechanisms.

