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The study found nonalcoholic fatty liver key mechanism

Recently, in the international academic journal Nature, a research team published a study on the progress of liver lipid metabolism regulation mechanism to date.

The liver is fatty acid oxidation and decomposition and synthesis of fatty acids and fatty important places in the digestion of lipids, absorption, decomposition, synthesis and transport and other metabolic processes play an important role in both. But the process of de novo synthesis of lipid enhancements to the accumulation of triglycerides in the liver abnormalities, leading to non-alcoholic fatty liver and insulin resistance happening.

SREBP1 lipid synthesis process is a very important transcription factors, after transcription and translation in an inactive state of the precursor form of the endoplasmic reticulum occurred in connection with the gene, insulin signal when cells are activated, SREBP1 will be dependent COPII transport pathway from the endoplasmic reticulum to the Golgi apparatus, through the Golgi processed to form an active protease inside the form, followed by nuclear cytoplasmic shuttling translocates to the nucleus to induce gene expression of lipid synthesis. But all along, in insulin resistance in obesity and diabetes, SREBP1 how enhanced activity, the mechanisms have been unclear.

In this study, researchers found that CREB transcriptional regulatory coactivator 2 (CRTC2) can be adjusted dependent COPII SREBP1 process, but this will be subject to regulatory action CRTC2 of mTOR signaling pathway. The researchers found that CRTC2 can compete with an important component in COPII complex combination of another component of the composite body, thereby disrupting SREBP1 transport. In the feeding process, mTOR phosphorylation able to CRTC2 weaken its inhibitory effect on COPII dependent SREBP1 processing pathway. In the liver of obese mice overexpressing mTOR phosphorylation can not be CRTC2 mutants can significantly alter the expression of genes of lipid synthesis, increasing insulin sensitivity.

In summary, this study found that CRTC2 can be suppressed by the impact COPII SREBP1 dependent protein lipid synthesis process, while CRTC2 will be regulated by mTOR signaling pathway, this finding to improve the non-alcoholic fatty liver disease, the development of related intervention means provides an important theoretical basis.