Lying just behind the stomach, measuring about the size of your hand, lies the pancreas; a small but mighty organ! The pancreas produces both digestive juices and enzymes but also is a crucial organ in maintaining blood glucose levels through the production and release of glucose-altering hormones. 

These hormones are secreted from specialised cells contained within cell clusters termed the “pancreatic islets‘. When blood glucose falls, glucose-raising glucagon is released from alpha-cells. The opposite is true when blood glucose levels rise, with glucose-lowering insulin being released from beta-cells to return blood glucose to normal. 

In type 2 diabetes, the balance of these hormones is thrown off, with insulin levels dropping and glucagon levels rising. This is coupled with progressive insensitivity to the actions of insulin, particularly in obesity. 

In order to meet metabolic demand and bring blood glucose under control our beta-cells are forced to work harder to produce ever-increasing quantities of insulin. That is, until they no longer can. 

Beta-cells can eventually become “burned-out” leading to cell-death. This forces remaining cell mass to continue to work harder until they are met with the same fate. 

Diabetes medications do not address this beta-cell decline, meaning many type 2 patients ultimately require insulin therapy. 

Dia Beta Labs are seeking to change this through development of our therapeutic pipeline. 

Dia Beta Labs are developing a pipeline of novel, peptide therapeutics which interact with previously untapped receptors on the beta-cell surface to prevent and reverse the loss of beta-cells in diabetes. 

Our therapeutic candidates have been validated in cellular and rodent models of diabetes. 

When injected with a beta-cell toxin, the clearly defined, circular structure of pancreatic islets becomes distorted and beta-cells are lost. This mirrors the pancreatic condition of severely diabetic patients. 

Following 28 days treatment with a DBL therapeutic peptide, the structure of pancreatic islets return to a normal, pre-diabetic state, highlighting true disease modification.