In a recent study, researchers found blocking a protein, VDAC1, in the insulin-producing beta cells, may help restore their normal function in case of type 2 diabetes.
In their experiments, the researchers also shown that it is possible to prevent the development of the disease.
The study was conducted by a team at Lund University in Sweden.
They believe that the active substance, which inhibits the protein VDAC1, could play a part in future drug development for the treatment of type 2 diabetes.
Their goal was to be able to administer the substance to newly diagnosed type 2 diabetics to allow the insulin-producing beta cells to retain their function.
Or, even better, to give it to pre-diabetics to prevent the onset of type 2 diabetes.
It is a small study based on cell donations from six deceased people with type 2 diabetes, as well as a limited number of experiments in animal models.
Further studies are needed to demonstrate how blocking VDAC1 affects kidney, heart, muscle and fat tissue, for example.
However, the results thus far have been so promising that we have patented the use of the active substance within the diabetes field.
Pre-diabetics may experience elevated blood glucose levels for many years before developing type 2 diabetes. High glucose levels initiate a series of negative processes.
Among other things, they increase the production of VDAC1, a so-called channel protein within the cells that, with the help of a substance, ATP, releases energy from the cell’s power plants, the mitochondria, to other parts of the cell, to be used for insulin secretion.
At constant high levels of glucose, however, the levels of the VDAC1 protein increase, causing VDAC1 to attach also to the cell surface.
The energy (ATP) then leaks out of the cell and causes cell death due to a lack of energy.
This, in turn, leads to impaired blood glucose control that eventually causes organ complications, such as cardiovascular disease, kidney disease, blindness and stroke.
When the researchers blocked VDAC1 in beta cells from organ donors with type 2 diabetes, the energy supply was restored and the insulin secretion was normalized.
The experiments were subsequently repeated on mice, which are known to develop genetically conditioned diabetes.
As a result, the disease did not develop and the insulin production was maintained for five weeks, at which point the treatment was discontinued and the glucose levels increased.
Further studies are needed to demonstrate how blocking of VDAC1 affects tissues such as kidneys, heart muscles and fat.
In addition to specific VDAC1 antibodies and VDAC1 inhibitors obtained in collaboration with Israeli researchers, the researchers in Lund also used the diabetes drug, metformin, and achieved the same effect.
The authors of the study point out that there is also a link between VDAC1 and Alzheimer’s disease, as high levels of VDAC1 can be found in brain cells in the parts of the brain that are affected at an early stage of the disease.
The findings are published in the scientific journal Cell Metabolism.
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