A development research study, collectively led by Professor Jang Hyun Choi and Professor Sung Ho Park from the Department of Biological Sciences at UNIST has recognized a key element implicated in the progression of non-alcoholic fatty liver disease (NAFLD), which is often activated by weight problems. NAFLD incorporates numerous metabolic diseases such as fatty liver disease and cirrhosis resulting from extreme fat build-up. Through animal experiments carried out on rats, the research study group showed that Thrap3 directly binds to AMPK within the liver. In essence, preventing Thrap3 expression presents an appealing opportunity for successfully dealing with NAFLD.
New research study reveals that the Thrap3 protein worsens NAFLD by interrupting fat metabolic process in the liver, suggesting that targeting Thrap3 could cause brand-new treatments for the disease.
An advancement study, collectively led by Professor Jang Hyun Choi and Professor Sung Ho Park from the Department of Biological Sciences at UNIST has recognized a crucial element implicated in the development of non-alcoholic fatty liver illness (NAFLD), which is often activated by obesity. The scientists discovered that a protein called Thrap3, which is associated with thyroid hormonal agent receptors, substantially gets worse NAFLD It does so by reducing the activity of adenosine monophosphate-activated protein kinase (AMPK), an essential regulator of fat metabolism in the liver.
Significance and Mechanism of Thrap3 in NAFLD.
NAFLD incorporates different metabolic diseases such as fatty liver disease and cirrhosis arising from extreme fat accumulation. Regardless of its prevalence, efficient treatments for NAFLD have actually been limited. However, this groundbreaking research study sheds light on possible restorative approaches.
A breakthrough research study, jointly led by Professor Jang Hyun Choi and Professor Sung Ho Park from the Department of Biological Sciences at UNIST has recognized a crucial aspect associated with the advancement of non-alcoholic fatty liver illness (NAFLD) triggered by weight problems. Credit: UNIST
Through animal experiments carried out on rats, the research study group showed that Thrap3 directly binds to AMPK within the liver. This interaction avoids AMPK from translocating from the nucleus to the cytoplasm and hinders autophagy– a procedure essential for breaking down triglycerides and reducing cholesterol levels. In essence, hindering Thrap3 expression provides an appealing avenue for successfully treating NAFLD.
Research Impact and Future Prospects
” We have encountered substantial obstacles while developing treatment strategies for non-alcoholic fatty liver illness. Our discovery of the Thrap3 gene offers us with an efficient approach to tackle this condition,” commented Professor Choi.
Schematic diagram of the mechanism by which Thrap3 affects NAFLD through translocation of AMPK. Credit: UNIST
Additionally, it was validated that suppressing Thrap3 expression efficiently improves non-alcoholic steatohepatitis– an inflammatory illness stemming from fatty liver.
Recommendation: “Thrap3 promotes nonalcoholic fatty liver disease by suppressing AMPK-mediated autophagy” by Hyun-Jun Jang, Yo Han Lee, Tam Dao, Yunju Jo, Keon Woo Khim, Hye-jin Eom, Ju Eun Lee, Yi Jin Song, Sun Sil Choi, Kieun Park, Haneul Ji, Young Chan Chae, Kyungjae Myung, Hongtae Kim, Dongryeol Ryu, Neung Hwa Park, Sung Ho Park and Jang Hyun Choi, 32 July 2023, Experimental & & Molecular Medicine.DOI: 10.1038/ s12276-023-01047-4.
Supported by funding from the Korea Research Foundation under the Ministry of Science and ICT, National Mouse Phenotype Analysis Group (KMPC), and UNIST Future Lead Project. Teacher Jang Hyun Choi, together with Professor Sung Ho Park, served as matching authors of the paper, with Dr. Hyun-Jun Jang and Dr. Yo Han Lee from the Department of Biological Sciences at UNIST participating as co-authors.
