Abstract
MicroRNAs (miRNAs), as a series of important short-chain non-coding RNAs, play an important post-transcriptional role in many biological activities, including adipogenesis. miR-144 is significantly upregulated in type II diabetes (T2D), and is considered to be an important biomarker for T2D. However, although the occurrence of T2D is inextricably linked to adipogenesis, whether miR-144 directly regulates adipogenesis remains to be further explored. In this paper, we demonstrate that miR-144 has a higher expression level in a porcine high backfat group, and it has a significant positive effect on promoting the differentiation of pre-adipocytes. FoxO1 is a target gene of miR-144, and inhibits the differentiation of pre-adipocytes. On the other hand, we demonstrate that FoxO1 can bind to the AdipoQ gene promoter, then regulate the AdipoQ expression by binding to the FoxO1 binding site in the AdipoQ promoter -1,499 to -1,489 bp and -1,238 to -1,228 bp regions, especially the -1,499 to -1,489 bp region. Meanwhile, miR-144 and FoxO1 co-expressional research has also shown that both factors regulate adipogenesis. To sum up, our research indicates that miR-144 targets FoxO1, thus reducing its expression and inhibiting its promotional effect on adiponectin, thereby alleviating the inhibitory effect of adiponectin on adipogenesis.
Highlights
Obesity has gradually become one of the major threats to human health around the world
As T2D is closely related to adipogenesis, and miR-144 is significantly upregulated in T2D, the role it plays still needs to be further investigated
These data were sequenced from the liver rather than adipose tissue, so we detected the miR-144 expression level in porcine white adipose tissue (WAT)
Summary
Obesity has gradually become one of the major threats to human health around the world. A batch of diseases such as type II diabetes (T2D), hypertension, and cardiovascular disease are closely related to being overweight or obesity (Kopelman, 2000; Goran et al, 2003). Adipocyte differentiation and proliferation lead to fat tissue expansion, and excessive fat tissue results in obesity-related metabolic syndromes. Adipocytes are emerging as a significant target in the treatment of obesity-related metabolic syndromes in the clinical setting (Shen et al, 2018). In this context, it is very necessary to explore the molecular genetic mechanisms of adipocyte differentiation and proliferation
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