miR-370-3p Regulates Adipogenesis through Targeting Mknk1.
Peiwen ZhangXinrong LiShunhua ZhangShuang WuQian XiaoYang GuXinyu GuoXutao LinLei ChenYe ZhaoLili NiuGuoqing TangYanzhi JiangLinyuan ShenLi ZhuPublished in: Molecules (Basel, Switzerland) (2021)
Excessive fat accumulation can lead to obesity, diabetes, hyperlipidemia, atherosclerosis, and other diseases. MicroRNAs are a class of microRNAs that regulate gene expression and are highly conserved in function among species. microRNAs have been shown to act as regulatory factors to inhibit fat accumulation in the body. We found that miR-370-3p was expressed at lower levels in the fat mass of mice on a high-fat diet than in mice on a normal control diet. Furthermore, our data showed that the overexpression of miR-370-3p significantly suppressed the mRNA expression levels of adipogenic markers. Thus, miR-370-3p overexpression reduced lipid accumulation. Conversely, the inhibition of miR-370-3p suppressed 3T3-L1 preadipocyte proliferation and promoted preadipocyte differentiation. In addition, Mknk1, a target gene of miR-370-3p, plays an opposing role in preadipocyte proliferation and differentiation. Moreover, consistent results from in vitro as well as in vivo experiments suggest that the inhibition of fat accumulation by miR-370-3p may result from the inhibition of saturated fatty acids that promote the accumulation of polyunsaturated fatty acids. In conclusion, these results suggest that miR-370-3p plays an important role in adipogenesis and fatty acid metabolism through the regulation of Mknk1.
Keyphrases
- fatty acid
- high fat diet induced
- high fat diet
- insulin resistance
- adipose tissue
- gene expression
- transcription factor
- type diabetes
- cardiovascular disease
- metabolic syndrome
- signaling pathway
- weight loss
- cell proliferation
- skeletal muscle
- weight gain
- dna methylation
- physical activity
- glycemic control
- electronic health record
- drug delivery
- wild type