Tsinghua University scientists found key mechanisms for the treatment of nonalcoholic fatty liver
July 10, 2015 Source: Bio Valley
Window._bd_share_config={ "common":{ "bdSnsKey":{ },"bdText":"","bdMini":"2","bdMiniList":false,"bdPic":"","bdStyle":" 0","bdSize":"16"},"share":{ }};with(document)0[(getElementsByTagName('head')[0]||body).appendChild(createElement('script')) .src='http://bdimg.share.baidu.com/static/api/js/share.js?v=89860593.js?cdnversion='+~(-new Date()/36e5)];It is well known that the liver plays an important role in the metabolic processes of lipid digestion, absorption, decomposition, synthesis and transportation. The liver is an important site for the oxidative decomposition of fatty acids and the synthesis of fatty acids and fats. However, due to the enhanced de novo synthesis of lipids, triglycerides accumulate abnormally in the liver, leading to non-alcoholic fatty liver and insulin resistance.
SREBP1 is a very important transcriptional regulator in lipid synthesis. After transcriptional translation, it binds to the endoplasmic reticulum in an inactive state. When cells are activated by insulin signaling, SREBP1 is COPII-dependent. The pathway is transported from the endoplasmic reticulum to the Golgi apparatus, and the active form is formed by processing the protease inside the Golgi apparatus, and then the nuclear transfer is transferred to the nucleus to induce the expression of the lipid synthesis gene. However, the activity of SREBP1 has been enhanced in insulin resistance to obesity and diabetes, and the mechanism has not been known.
In this study, the researchers found that CREB transcriptional regulatory coactivator 2 (CRTC2) regulates COPII-dependent SREBP1 processing, and that this role of CRTC2 is also regulated by the mTOR signaling pathway. The researchers found that CRTC2 competes with an important component of the COPII complex for binding to another component of the complex, thereby disrupting the transport of SREBP1. During feeding, mTOR is able to phosphorylate CRTC2, attenuating its inhibitory effect on the COPII-dependent SREBP1 processing pathway. Overexpression of a CRTC2 mutant that is not phosphorylated by mTOR in the liver of obese mice can significantly alter the expression of lipid synthesis genes and increase insulin sensitivity.
Taken together, this study found that CRTC2 inhibits lipid synthesis by affecting COPII-dependent SREBP1 protein processing, and that CRTC2 is also regulated by the mTOR signaling pathway, a finding that is related to improving nonalcoholic fatty liver disease. Interventions provide an important theoretical basis.
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