In groundbreaking diabetes research over the past two decades, Anath Shalev, M.D., has shown that the protein TXNIP regulates survival and function of beta cells, the pancreatic cells that produce the hormone insulin to lower levels of glucose in the blood. Downregulation or inhibition of TXNIP in beta cells protects against diabetes in mouse models, and a repurposed clinical drug that inhibits TXNIP shows promising results in people with recent-onset Type 1 diabetes.

Beta cells play a key role in the pathogenesis of both Type 1 and Type 2 diabetes. However, pancreatic islets also have alpha cells that produce the hormone glucagon, which acts to raise glucose blood levels. Together, insulin and glucagon keep blood glucose levels stable. 

To further understand the role of TXNIP in pancreatic islet biology and glucose control, Shalev and colleagues at the University of Alabama at Birmingham now report the effect of knocking out TXNIP in alpha cells.

While not as dramatic as beta-cell TXNIP knockouts, the alpha-cell knockout improved diabetes-associated hyperglycemia and hyperglucagonemia in a mouse model of streptozotocin-induced diabetes. Hyperglycemia and hyperglucagonemia — excess levels of glucose and glucagon in the blood — are hallmarks of diabetes.

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