Diabetes of all types is an ever-increasing problem worldwide. As a condition, it truly impacts every aspect of a patient’s life, and there is growing pressure to find solutions to help curb the trend. Regardless of the specific type, a key hallmark of the disease is β-cell dysfunction, demonstrated by insufficient insulin release in response to hyperglycaemia. Much of the focus for research has been on slowing the decline or even reversing this dysfunction.

Shi et al. used a protein named C-type lectin domain containing 11A (CLEC11A), also known as stem cell growth factor, C-type lectin superfamily member 3 or osteolectin 1, to attempt to prevent β-cell dysfunction. This is a secreted sulfated glycoprotein that is highly expressed in bone marrow. Remarkably, not only is this protein expressed within both α- and β-cells of the pancreas, long term treatment with exogenous recombinant human CLEC11A (rhCLEC11A) accentuated glucose-stimulated insulin secretion, insulin content and proliferation of human islet cells.

Using cell culture models and combined physiological testing, the group was able to demonstrate a 1.5-fold increase in islet content of insulin and improvement in the overall insulin content of close to 50%. Additionally, the group began to show some interesting links with levels of protein and levels of obesity, indicating a potential causal relationship between type 2 diabetes and obesity which may lead to a new way of thinking about the condition.

This could be the next new hope for those with diabetes and could potentially provide a novel therapeutic target for maintaining insulin production from within pancreatic β-cells in those with dysfunction. It is certainly a timely article which should be of interest to all endocrinologists.

Read the full article in Journal of Molecular Endocrinology 71 e220066