The research, led by Prof. Yuval Dor, is defined as a breakthrough in the fight against diabetes, and is the product of a long process
Researchers from the Hebrew University have identified the key to the production of beta cells responsible for the production of insulin in the pancreas. The discovery is a breakthrough that may eventually help researchers find ways to restore or increase the function of beta cells in people suffering from juvenile or adult diabetes.
The work on the long-term project was led by Prof. Yuval Dor from the Israel-Canada Medical Research Institute of the Hebrew University, researchers from the Hadassah Medical Center and in collaboration with research groups from universities in the USA and the pharmaceutical company Roche. The study was recently published in the journal Cell Metabolism.
"Our work showed that when the glucose level in the blood rises, it causes the division of beta cells," explains Prof. Dor. "However, the key is not the glucose in the blood directly, but the rate of its breakdown within beta cells. This breakdown is controlled by a key enzyme in beta cells, glucokinase, and the discovery therefore points to this enzyme as a target for developing drugs that will increase the production rate of beta cells. In fact, because drugs that already activate glucokinase are already in clinical development, so the path to implementation may be shorter."
The immune system of people suffering from juvenile diabetes mistakenly attacks the beta cells that produce insulin to the point of their complete destruction. Without insulin, the body's cells are unable to absorb the glucose from the blood and use it to create energy, and remain starved. At the same time, glucose accumulates in the blood and may cause long-term complications such as kidney failure and blindness. For this reason, people suffering from the disease must inject insulin and monitor their blood glucose level strictly and continuously. In order to cure juvenile diabetes, it will be necessary to develop new methods to increase beta cell production, hence the therapeutic potential of this research. Adult diabetes is a more complex and much more common disease, but even in this disease the lack of beta cells is a critical factor.
In their work, Prof. Dore and Prof. Benjamin Glazer from the Hadassah Medical Center used a genetic system to destroy 80 percent of the insulin-producing cells in the pancreas of adult mice, thus causing them to develop diabetes. When the researchers compared these mice to another group of mice that served as the control group of the experiment, it was found that the diabetic mice with the high blood glucose level created a greater number of new beta cells compared to healthy control mice. The finding suggested that glucose may play a key role in beta cell regeneration. In the next phase of the research, the researchers found that glucokinase is the molecule that plays a central role in the regeneration process of beta cells.
"This means that the harder beta cells are required to work, the more they produce of themselves," explains doctoral student Shai Porat who, together with doctoral student Noa Weinberg-Koram, led the research, which was funded with the support of the Juvenile Diabetes Research Fund.
Since the research showed that cell regeneration depends on the activity of the glucokinase enzyme, the discovery may pave the way for the development of a new type of drug that will increase the number of beta cells in the body (regeneration) by accelerating their replication. This is based on molecules, currently under development, that increase the activity rate of glucokinase. Such drugs could help increase the mass of beta cells in adult diabetics. Combined with tools that will be developed in the future to block the attack of beta cells by the immune system, the combined treatment could pave the way for a full cure for juvenile diabetes patients.
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Totally a million breakthroughs when will the patients be cured diabetes has ruined their lives and all the time the hope is like beautiful sparkling soap bubbles that you come to hurt and fade away as if we weren't there in 2023 I thought in the year XNUMX some diseases will have been eradicated and still all the trillions and science just brags every day about inventions and breakthroughs Through dramatics and all and everything in one big bluff that seems alive, drawing imaginary budgets and each time releasing some kind of hope and there is no warmth behind all the breakthroughs Wait a second I went to read another article?
Two main questions that arose for me from the article:
1. It is written in the article that the percentage of beta cells destroyed in the mice is about 80%, I remember, I may be wrong, that the destruction of beta cells in type 1 diabetics which is 80% is still defined as the "honeymoon" period. If so, combined treatment of glucose and preparations that accelerate the production of glucokinase are only effective for new type 1 diabetics who are still in the honeymoon period and/or for patients with type 2 diabetes?
2. Does your research also concern the immune system's attack on the beta cells?
Because, even if you manage to create such a treatment, which I assume, aims to replace most if not all of the insulin treatment, then the need for this treatment will also be required for the entire life of the diabetic. So what is the advantage of this over the usual treatment with the various insulins, pumps, and the artificial pancreas (when it goes on the market)?
That is, how will you turn the treatment into a treatment that is "non-chronic"?
magnificent! Sweet article
There is no fear that this will encourage an increase in the risk of pancreatic cancer?
It is not clear what the mechanism is in the end. I understood that the beta cells replicate themselves the more glucose there is in the blood and somehow glucokinase is related to this, but what is the mechanism actually, which is the essence of all this information, it is not explained at all!