Study Finds New Way To Regenerate Insulin-Producing Cells To Treat Diabetes

A study has found a new way to regenerate insulin-producing cells to treat diabetes in the form of MNK2 protein. The MNK2 protein could serve as a source of insulin for both type 1 and type 2 diabetes.

Study Finds New Way To Regenerate Insulin-Producing Cells To Treat Diabetes

A novel possible treatment target for diabetes has been identified by a Swedish researcher. In zebrafish larvae, laboratory pigs, and human cell cultures, inhibition of the protein MNK2 led to the regeneration of pancreatic insulin-producing cells.

According to Dr. Olov Andersson, senior researcher at the Department of Cell and Molecular Biology at the Karolinska Institute, “our findings indicate a new potential target for treating diabetes, in that we demonstrate a possible way of stimulating the formation of new insulin-producing cells.”

According to the study (read below), regeneration of insulin-producing beta cells in the pancreas occurred when the MNK2 protein was completely removed or inhibited in zebrafish cells.

Insulin is produced by beta cells, which are found in the pancreas. Insulin is a hormone that controls blood sugar levels by telling cells to take in blood sugar. This usually happens after a meal when blood sugar levels are at their highest.

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A chemical known as CID661578 was shown to be able to trigger the regeneration of pancreatic beta cells that produce insulin in the researcher’s earlier studies.

Instead of directly influencing the proliferation pathway, the current investigation discovered that CID661578 boosted beta cell regeneration by reducing the activity of MNK2 proteins.

CID661578 interacted with MNK2, preventing MNK2 from engaging with additional proteins involved in protein-generation mechanisms, which would later result in beta cell regeneration.

By doing this, CID665178 was successful in regenerating pancreatic beta cells in zebrafish larvae and zebrafish cell cultures.

Additionally, CID665178 molecules’ exposure to mammalian cell cultures revealed that pig and human cells could also experience the same effects.

Human organoids, which are cell cultures made to imitate organs, as well as pig pancreatic cell assays all experienced a rise in pancreatic beta cell proliferation after being treated with CID665178.

Although this role “warrants further investigation in diabetes,” the authors noted their work “demonstrates a targetable role of MNK2” in beta cell regeneration.

If effective, the MNK2 protein could serve as a source of insulin for both type 1 and type 2 diabetes.

In those with type 1 diabetes, the immune system accidentally kills beta cells, which reduces the number of beta cells and the amount of insulin produced. Beta cells progressively lose their capacity to generate insulin in type 2 diabetes as a result of decreased insulin signaling and cells that are no longer receptive to insulin.

Because both type 1 and type 2 diabetes patients require insulin injections to regulate their blood sugar levels, targeted MNK2 suppression for these patients could allow for the restoration of natural insulin production in the body through beta cell regeneration, allowing for more refined blood sugar regulation.

“We’ll now be studying the effect of this and similar molecules in human tissue and analyzing the molecule’s target protein, MNK2, in tissue from healthy donors and donors with diabetes,” said Andersson.

Read the study below:

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