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    Home > Active Ingredient News > Study of Nervous System > Nature cover article: nicotine addiction or increased risk of type 2 diabetes!

    Nature cover article: nicotine addiction or increased risk of type 2 diabetes!

    • Last Update: 2019-10-19
    • Source: Internet
    • Author: User
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    October 19, 2019 / BIOON / - recently, in a research report published in the international journal Nature, researchers from Mount Sinai Medical College found a special circuit in the body of rats through research, or linked smoking and the risk of type 2 diabetes Compared with non-smokers, diabetes is more prevalent in smokers, but the reasons behind it are not clear to researchers In this paper, the researchers found that the intake of nicotine may be related to the activity of the pancreas through a kind of brain circuit The intake of nicotine will cause the pancreas to release a small amount of insulin, thus increasing the blood glucose level of the body The higher blood glucose level is directly related to the increased risk of diabetes Source: cc0 public domain researchers found that diabetes The specific protein encoded by the related gene TCF7L2 (transcription factor 7 analogue 2) can mediate a signal circuit, thus connecting the neurons activated by nicotine with the regulation of pancreatic blood glucose; nicotine can activate the nicotinic acetylcholine receptor (nAChR) expressed by neurons in the medial habenular nucleus of the brain, thus causing the adverse reactions of nicotine To limit the absorption and release of glucagon and insulin by the pancreas, so as to improve the blood glucose level; higher blood glucose level can produce a feedback circuit by inhibiting the neurons expressing nAChR, block the negative effects of smoking, and help to establish nicotine dependence; TCF7L2 can regulate the whole signal circuit, and associate nicotine addiction with high risk of diabetes Researcher Paul J Kenny said the study is important because it describes a special mechanism that can control nicotine addiction, the same addiction related brain circuits or promote smoking related diseases (previously thought to be related to tobacco activity outside the brain) At least some of the pathogenicity of nicotine is produced in the brain by the same circuit controlling drug addiction, which means that in some cases, tobacco addiction and pathogenicity may have exactly the same potential mechanism Previous studies have shown that TCF7L2 can regulate gene expression in pancreas and liver In order to investigate the relationship between TCF7L2, nicotine addiction and blood glucose regulation, the researchers removed TCF7L2 from rats Compared with normal rats, the mutant rats can take more nicotine, and the removal of TCF7L2 will lead to the decrease of nicotine receptor level in the medial habenular nucleus, thus reducing the level of nicotine receptor in the medial habenular nucleus The ability of nicotine to activate aversion circuit in habenular region The loss of TCF7L2 function in this area will increase the intake of nicotine in rats, reduce the increase of nicotine driven blood glucose level, and protect the body against diabetes related abnormal blood glucose level This study revealed the relationship between nicotine intake and the development of type 2 diabetes If the results in rats can be extended to human population, the change of TCF7L2 gene will affect the risk of nicotine addiction and tobacco related type 2 diabetes The results of this study show that the development of type 2 diabetes may originate from the brain, and nicotine may interfere with the brain The interaction between the lateral habenular nucleus and the peripheral nervous system The results of this study are expected to help researchers find new ways to quit smoking, and special circuits in the brain can be used as a new target to help develop new treatments for diabetes in smokers Original source: Alexander Duncan, Mary P Heyer, masago Ishikawa, et al Habenular TCF7L2 links niche addition to diabetes, nature (2019) doi: 10.1038/s41586-019-1653-x
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