Scientists identify T-cadherin as a factor that feeds back a lack of insulin to pancreatic β cells and induces their proliferation, with the potential for treating diabetes. Wake up pancreas, it’s time for work! Researchers led by Osaka University in Japan have now identified a mechanism by which
Researchers identified a mechanism by which a lack of insulin may be reported back to the pancreatic cells that produce insulin, identifying a potential new therapeutic target for diabetes.
Wake up pancreas, it’s time for work! Researchers led by Osaka University in Japan have now identified a mechanism by which a lack of insulin may be reported back to the pancreatic cells that produce insulin. This discovery presents a potential new therapeutic target for diabetes. When the pancreas is unable to supply sufficient insulin, type 2 diabetes occurs. Insulin is the hormone that controls sugar use and storage, to meet physiological demands. If the body’s demand for insulin is not being met, the cells in the pancreas that make insulin, known as β cells, can usually proliferate to increase their numbers. However, it is unknown what factors are released from the insulin-receiving tissues or cells to signal the lack of insulin to the pancreatic β cells.
However, the researchers showed that T-cadherin is also secreted in previously undescribed soluble forms and can act as a humoral factor, i.e., a molecule transported through the circulatory system. They not only recognized that T-cadherin responds to insulin deficiency but also demonstrated that mice that were genetically engineered to lack T-cadherin had an impaired glucose tolerance when fed with a high-fat diet.
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