Metabolic syndrome is a fundamental health problem worldwide induced by obesity and T2DM. Obesity linked long-standing diabetes was established as a crucial event in cancer development. The recent findings improved that betatrophin, regulates lipid and glucose metabolism. However, the potential function of betatrophin activity in the pathogenesis of hepatocellular carcinoma (HCC) due to metabolic syndrome is not fully understood. This preliminary study aimed to elucidate the fundamental role of betatrophin in HCC linked metabolic syndrome. This study was conducted by in vivo model by using miR-122a-/- mouse induced by a high-fat diet. The alteration of liver betatrophin expression was confirmed by RT-qPCR method, while the histological section examination was done to observe the change of liver anatomy. Importantly, our study found that diet-induced obesity (DIO) was able to accelerate metabolic syndrome. The long-term treatment of DIO exacerbate portal inflammation, fatty liver and liver fibrosis accelerate liver tumorigenesis or precancer symptoms. The expression of betatrophin significantly increased in our metabolic syndrome mouse model indicate the involvement of betatrophin in lipid metabolism disorder to induce liver injury and hepatoma. Hence, this preliminary study proves a hallmark of the primary contribution of betatrophin in the early incidence of hepatocellular carcinoma linked metabolic syndrome.
|Journal||Journal of Physics: Conference Series|
|State||Published - 7 Jan 2019|
|Event||5th International Conference on Advanced Molecular Bioscience and Biomedical Engineering 2018, ICAMBBE 2018 - Malang, Indonesia|
Duration: 3 Sep 2018 → 4 Sep 2018