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Researchers Found the Molecular Mechanism of Genetic Predisposition to Type II Diabetes

2016-12-12 来源:转载自第三方
12 December 2016
   Recently, New Zealand scientists Peter R. Shepherd and his colleagues published a study "A Critical Role for β-Catenin in Modulating Levels of Insulin Secretion from β-Cells by Regulating Actin Cytoskeleton and Insulin Vesicle Localization"[1] in Journal of Biological Chemistry. It is the first time to discover the crucial role of β-catenin in the control of insulin release and the molecular mechanism of insulin release. This provides a new direction for the further study of genetic susceptibility to type II diabetes mellitus.
A Critical Role for β-Catenin in Modulating Levels of Insulin Secretion from β-Cells by Regulating Actin Cytoskeleton and Insulin Vesicle Localization
  Diabetes is a group of metabolic diseases characterized by hyperglycemia, the body of patients with type II diabetes can not produce enough insulin, and can not identify the insulin in body, resulting in increased blood glucose levels. In the study of type II diabetes, a variety of clear genetic mutations have been identified, such as insulin gene, insulin receptor gene, glucokinase gene, mitochondrial gene and so on. However, The processes regulating glucose-stimulated insulin secretion (GSIS) and its modulation by incretins in pancreatic β-cells are only partly understood.
  In this study, scientists studied the role of β-catenin in the process described above. TCF7L2 gene is a transcriptional coactivator of β-catenin, which is already known by the scientific community for a long time. Its mutations are one of the greatest contributors, and researchers have focused on the interaction of this gene with β-catenin to make sure whether individuals are genetically predisposed to type II diabetes.
  TCF7L2 can directly interact with β-catenin, β-catenin regulates the insulin levels in body, so as to ensure that the body has the appropriate level of insulin at the right time, which declares that drugs increases β-catenin Level in short-term will increase the secretion of insulin; Below the cell membrane, there are multi-layer actin fibers, these fibers can form a network binding with insulin, researchers found that β-catenin can control the network of actin fibers, and the characteristics of the fiber network can be changed by opening the gaps of the fiber network. This mechanism can help control the function of insulin, glucose metabolism in fat cells and the release of hormones in the brain.
  At present, about 50%~60% of individuals susceptible to type II diabetes have some genetic changes, making them more susceptible to diabetes. The current therapeutic agents for diabetes include α-glucosidase inhibitors, metformin, sulfonylurea glnidones, thiazolidinediones, GLP-1 analogs, and DPP-4 inhibitors such as vildagliptin (intermediate 3-amino-1-adamantanol), are the control agents of blood glucose. This study sheds light on the association between this mechanism of β-catenin and insulin release for the first time and provides direction and theoretical basis for how to control insulin release by manipulating β-catenin and finding new drugs for the treatment of type II diabetes.
[1] Brie Sorrenson, Emmanuelle Cognard, Kathryn L. Lee, et al. A Critical Role for β-catenin in Modulating Levels of Insulin Secretion from β-cells by Regulating Actin Cytoskeleton and Insulin Vesicle Localization. J. Biol. , Doi: 10.1074/jbc.M116.758516
Related links: 3-amino-1-adamantanol
                       The Mechanism and Common Drugs of DPP-4 Inhibitors
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