Researchers from Wuhan University, Chinese Academy of Medical Sciences and Peking Union Medical College confirmed that interferon regulatory factor 3 (IRF3) reduced liver steatosis and insulin resistance by inhibiting the IKKβ / NF-κB signaling pathway. Related research papers have been accepted and published online in the internationally renowned liver disease journal Hepatology (the latest impact factor 12.003).
Leading this research is Professor Hongliang Li, deputy director of the Institute of Cardiovascular Diseases of Wuhan University. Mainly engaged in the research of cardiovascular diseases, especially in heart diseases including myocardial hypertrophy, myocardial infarction, viral myocarditis and heart failure. He has published 42 academic papers at home and abroad, and the total number of citations of published papers in SCI source journals is> 350 times.
Obesity is an epidemic in modern industrial society. With changes in diet and lifestyle, the incidence of obesity is increasing year by year. In 2008, approximately 1.5 billion people worldwide were overweight and obese. It is estimated that by 2030, the number of overweight and obese people will reach 2.16 billion and 1.12 billion, respectively. Obesity can lead to confusion in the blood levels of insulin, sugar and blood lipids, and these problems can lead to various metabolic diseases such as hypertension, type 2 diabetes, non-alcoholic fatty liver disease and atherosclerosis. Obesity can also increase the risk of different types of cancer.
At present, obesity and related metabolic diseases are widely prevalent worldwide, and cause huge medical and economic burdens. Therefore, it is necessary to clarify the pathogenesis and pathological mechanism of obesity and related metabolic diseases, and find out their preventive measures.
In the past, Li Hongliang's group observed that interferon regulatory factors (IRFs) play a role in metabolic regulation, which prompted them to investigate the relationship between an important family member IRF3 and metabolic diseases. In this new article, the researchers confirmed that IRF3 expression is reduced in the livers of diet-induced and genetically obese subjects. Systemic IRF3 knockout (KO) significantly promoted liver insulin resistance and steatosis induced by chronic high-fat diet (HFD); in contrast, they found that adenovirus-mediated liver IRF3 overexpression can maintain glucose and liposomes in vivo Steady state. And overexpression of liver IRF3 reduced the increased systemic and liver inflammation in IRF3 KO mice.
Importantly, the researchers confirmed that IRF3 significantly inhibited the IKKβ / NF-κB signaling pathway, while overexpression of IκBα in the liver could reverse HFD-induced insulin resistance and steatosis in IRF3 KO mice. Mechanism research confirmed that IRF3 interacts with the IKKβ kinase domain in the cytoplasm, inhibiting its downstream signals. Furthermore, the absence of the region responsible for IRF3 / IKKβ interaction in IRF3 inhibits IRF3's ability to maintain glucose and lipid homeostasis.
These findings indicate that IRF3 inhibits IKKβ / NF-κB signaling by interacting with IKKβ in the cytoplasm, thereby reducing liver inflammation, insulin resistance and hepatic steatosis.
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