Study Finds New Way to Regenerate Insulin-Producing Cells to Treat Diabetes
A Swedish study has found a new potential therapeutic target for diabetes. Inhibition of a protein named MNK2 regenerated pancreatic insulin-producing cells in zebrafish larvae, laboratory pigs, and human cell cultures.“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,” said Dr. Olov Andersson, senior researcher at the Department of Cell and Molecular Biology at Karolinska Institute. The study found that inhibition, or complete removal of the MNK2 protein in zebrafish cells, resulted in the regeneration of insulin-producing beta cells in the pancreas. Beta cells reside in the pancreas and are responsible for producing insulin. Insulin is a hormone that regulates blood sugar levels by signaling to cells to take in blood sugar, commonly after a meal when the sugar levels become high. The researcher’s previous study identified a molecule named CID661578 that was able to stimulate the regeneration of pancreatic insulin-producing beta cells. The current study, however, found that CID661578 stimulated beta cell regeneration by inhibiting the action of MNK2 proteins rather than playing a direct role in the proliferation pathway. By interacting with MNK2, CID661578 prevented MNK2 from interacting with other proteins involved in protein-generation pathways, which would induce beta cell regeneration downstream. In doing so, CID665178 was able to regenerate pancreatic beta cells in zebrafish larvae and zebrafish cell cultures. Further, exposure of CID665178 molecules on mammalian cell cultures demonstrated that the same effects could also be crossed over in pig and human cells. Pig pancreatic cell assays and human organoids—cell cultures that resemble an organ—all saw increased growth of pancreatic beta cells after being treated with CID665178. The authors said that their study demonstrates a “targetable role of MNK2” in beta cell regeneration, though this role “warrants further investigation in diabetes.” If successful, the MNK2 protein may be a suitable therapeutic target for both type 1 and type 2 diabetes as a source of insulin. In type 1 diabetes, the immune system mistakenly attacks beta cells and kills them, leading to a loss of beta cells and insulin production. Whereas in type 2 diabetes, insulin signaling becomes impaired with cells becoming unresponsive to insulin, resulting in beta cells gradually losing their ability to produce insulin. Since both type 1 and type 2 diabetes patients require insulin injections for blood sugar regulation, targeted MNK2 inhibition for these patients may allow restoration of natural insulin production in the body through beta cell regeneration, which will allow a more nuanced regulation of blood sugar levels. “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.
Udumbara
A Swedish study has found a new potential therapeutic target for diabetes. Inhibition of a protein named MNK2 regenerated pancreatic insulin-producing cells in zebrafish larvae, laboratory pigs, and human cell cultures.
“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,” said Dr. Olov Andersson, senior researcher at the Department of Cell and Molecular Biology at Karolinska Institute.
The study found that inhibition, or complete removal of the MNK2 protein in zebrafish cells, resulted in the regeneration of insulin-producing beta cells in the pancreas.
Beta cells reside in the pancreas and are responsible for producing insulin. Insulin is a hormone that regulates blood sugar levels by signaling to cells to take in blood sugar, commonly after a meal when the sugar levels become high.
The researcher’s previous study identified a molecule named CID661578 that was able to stimulate the regeneration of pancreatic insulin-producing beta cells.
The current study, however, found that CID661578 stimulated beta cell regeneration by inhibiting the action of MNK2 proteins rather than playing a direct role in the proliferation pathway.
By interacting with MNK2, CID661578 prevented MNK2 from interacting with other proteins involved in protein-generation pathways, which would induce beta cell regeneration downstream.
In doing so, CID665178 was able to regenerate pancreatic beta cells in zebrafish larvae and zebrafish cell cultures.
Further, exposure of CID665178 molecules on mammalian cell cultures demonstrated that the same effects could also be crossed over in pig and human cells.
Pig pancreatic cell assays and human organoids—cell cultures that resemble an organ—all saw increased growth of pancreatic beta cells after being treated with CID665178.
The authors said that their study demonstrates a “targetable role of MNK2” in beta cell regeneration, though this role “warrants further investigation in diabetes.”
If successful, the MNK2 protein may be a suitable therapeutic target for both type 1 and type 2 diabetes as a source of insulin.
In type 1 diabetes, the immune system mistakenly attacks beta cells and kills them, leading to a loss of beta cells and insulin production. Whereas in type 2 diabetes, insulin signaling becomes impaired with cells becoming unresponsive to insulin, resulting in beta cells gradually losing their ability to produce insulin.
Since both type 1 and type 2 diabetes patients require insulin injections for blood sugar regulation, targeted MNK2 inhibition for these patients may allow restoration of natural insulin production in the body through beta cell regeneration, which will allow a more nuanced regulation of blood sugar levels.
“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.
