According to a recent study, published in the journal Nature Communications, researchers discovered therapeutic targets for the conservation and restoring of beta cells, the cells present in the pancreas that produce and divide insulin in the body. The study's findings could be a life changing development for patients suffering from type 2 diabetes. The discovery of therapeutic targets may help a lot of people globally by preventing insulin resistance. The study was led by researchers from Diabetes, Obesity and Metabolism Institute (DOMI) at the Icahn School of Medicine at Mount Sinai.
All the main types of diabetes are caused due to inadequate b-cell mass. When blood glucose levels increase in the body, because of a high-fat diet, b cells give response by producing more insulin to control the blood glucose levels. However, persistent high high blood sugar levels, a condition called hyperglycemia, can affect the function of B cells to produce and release insulin. This leads to an impact on the cycle of increasing glucose levels and ever-reducing b-cell function, causing b-cell death, also known as glucose toxicity. Therefore, conservation and regeneration of b cells is a therapeutic target for diabetes.
The researchers found out that it was possible to manage the effects of ChREBPb and the b-cell death they noticed by increasing expression of a different type of the protein, ChREBP, or by activating nuclear factor-erythroid factor 2 (Nrf2), which is a protein that defends cells caused by oxidative damage in both mice and human b cells, hence restoring b-cell mass.
Donald Scott, PhD, a Professor of Medicine (Endocrinology, Diabetes and Bone Disease) at Icahn Mount Sinai, and a member of DOMI and of The Mindich Child Health and Development Institute, said, "Traditionally, ChREBP was thought to be a mediator of glucose toxicity, but we noticed one form, ChREBPa, appeared to protect beta cells." He further added, "By using tools we developed that enabled us to interrogate these isoforms independently, we found that ChREBPb plays a key role in the gradual destruction of b cells. Thus, we believe it is a marker of hyperglycemia and glucose toxicity."
He said, "Moreover, we found that if you remove ChREBPb or counteract it pharmacologically, you can mitigate the effects of glucose toxicity and protect those cells. This exciting discovery creates an opportunity to develop therapeutic agents that target this molecular mechanism, effectively block ChREBPb production, and thus preserve b-cell mass. This would not only address the challenge that has driven diabetes research for years but also prevent patients with type 2 diabetes from becoming insulin dependent due to loss of b-cell mass, which would have a significant impact on outcomes and quality of life."