Our superhero, pancreas, needs some help!

Osaka University researchers

have discovered a mechanism through which a lack of insulin can be
transmitted back to the pancreatic cells that create insulin, revealing a potential
new therapeutic target for diabetes.
Type 2 diabetes affects an estimated 400 million individuals globally, and insulin control in the body is
still remain unclear. Type 2 diabetes develops when the pancreas fails to produce enough insulin, the
hormone that regulates sugar utilization and storage, to meet physiological demands. If the body's
demand for insulin is not met, the cells in the pancreas that create insulin can normally multiply to
increase their numbers. It is uncertain, however, what substances are released by insulin-receiving
tissues or cells to indicate a shortage of insulin to pancreatic cells.
Researchers discovered that a protein called T-cadherin may be involved in providing feedback to
insulin-producing pancreatic cells and modulating their proliferation in a study published in iScience.
T-cadherin is often found on the cell surface and is best recognized as the binding partner for
adiponectin, a protein released particularly by fat-storing cells. T-cadherin, on the other hand, is
secreted in heretofore unrecognized soluble forms and can function as a humoral factor, or a molecule
conveyed through the circulatory system, according to the researchers. They not only discovered that
T-cadherin responds to insulin deficit, but they also discovered that mice genetically modified to lack
T-cadherin had poor glucose tolerance when fed a high-fat diet.
"RNA sequencing analysis, which was utilized to investigate genome-wide gene expression levels,
indicated lower expression of Notch signaling proteins in cells from mice lacking T-cadherin," lead
scientist Tomonori Okita and corresponding author Shunbun Kita explain. These proteins are thought
to have a role in the Notch signaling system, which promotes -cell proliferation; this suggests that
soluble T-cadherin stimulates pancreatic β-cells to boost insulin production via the Notch pathway.
"We then used artificially synthesized T-cadherin to treat isolated mouse pancreatic islets, which are
β cells production regions of the pancreas," says senior author Iichiro Shimomura. "This therapy
increased Notch signaling in mouse islets, which could lead to β -cell proliferation." These findings are
exciting because they suggest that T-cadherin could be used in the fundamental treatment of diabetes.