Study finds small RNA regulates insulin sensitivity by targeting Sirt1 gene
Recently, the international academic journal Diabetologia published online the research paper Downregulation of miR-181aupregulates sirtuin-1 (SIRT1) and improves hepatic insulin sensitivity of the Institute of Nutrition, Shanghai Institute of Life Sciences, Chinese Academy of Sciences. The study found that inhibiting the non-coding small RNA miR-181a can up-regulate the protein level of deacetylase SIRT1 and improve insulin resistance.
Insulin resistance is a key factor leading to type 2 diabetes. Insulin resistance occurs when the liver, skeletal muscle, adipose tissue, etc., the target organs of insulin, respond weakly to insulin. Alleviating insulin resistance is an important way to prevent and treat type 2 diabetes. A preliminary study by Zhai Qiwei's research group found that protein deacetylase SIRT1 can improve insulin sensitivity by inhibiting PTP1B expression at the chromatin level, and found that resveratrol present in foods such as grapes and blueberries can improve insulin sensitivity through SIRT1 (Cell Metabolism, 2007; 6 (4): 307-19). At present, SIRT1's regulation of insulin sensitivity has been widely recognized by international colleagues, but how SIRT1 itself is regulated under physiological and pathological conditions, and the mechanism of further affecting insulin sensitivity is not yet clear.
Zhai Qiwei's research group PhD students Zhou Ben and Li Cheng found that a non-coding small RNA miR-181a can target the 3 'untranslated region of Sirt1 mRNA and inhibit SIRT1 translation, but does not affect its transcription. In the cell and animal models of insulin resistance, the level of miR-181a was significantly increased, and the level of miR-181a in the serum of diabetic patients was also significantly increased. Cell experiments have shown that overexpression of miR-181a can reduce SIRT1 protein levels and induce insulin resistance; while inhibition of miR-181a in insulin resistance can increase SIRT1 protein levels and enhance insulin sensitivity. Furthermore, using adenoviruses that overexpress SIRT1 and SIRT1 gene knockout mice, it was found that the regulatory effect of miR-181a on insulin sensitivity depends on SIRT1.
Further research found that overexpression of miR-181a in mice can lead to insulin resistance and glucose metabolism disorders, and a high-fat diet-induced insulin resistance mouse model was injected with locked nucleic acid modified miR-181a antisense nucleic acid (anti-miR-181a ) To inhibit miR-181a can effectively increase the SIRT1 protein level, and improve the body's glucose tolerance, liver and muscle insulin sensitivity, and lower blood sugar levels.
These research results show that miR-181a may become a diagnostic or typing marker for insulin resistance-related diseases (such as type 2 diabetes, etc.), and a drug target for treatment.
The research was funded by the Chinese Academy of Sciences, the National Natural Science Foundation of China, the Ministry of Science and Technology, and the Shanghai Municipal Science and Technology Commission.
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