Washington: Researchers have confirmed the potential of a protein for the treatment of type 2 diabetes.
Researchers at the Institute for Research in Biomedicine (IRB Barcelona) have discovered that deficiency of a single protein, Mitofusin 2, in muscle and hepatic cells of mice is sufficient to cause tissues to become insensitive to insulin, thus producing an increase in blood glucose concentrations.
These are the two most common conditions prior to development of diabetes type 2.
The study validates Mitofusin 2 as a possible target for the treatment of diabetes type 2.
“Resistance to insulin plays a key role in the development of diabetes mellitus, dyslipidemia (alteration of lipid concentrations) and obesity. Mitofusin 2 may provide a specific target for the development of drugs that could hold back a disease that affects millions of people worldwide”, explains the head of the study, Antonio Zorzano, full professor of the University of Barcelona, coordinator of the Molecular Medicine Programme at IRB Barcelona, and head of the Heterogenic and Polygenic Diseases lab at the same centre.
Previous studies performed at IRB Barcelona demonstrate that both obese and diabetes type 2 subjects have low levels of muscle Mitofusin 2.
This protein controls the insulin signalling pathway in the liver and muscles.
The scientists have observed that deficiency of this protein causes alterations in mitochondria and the endoplasmic reticulum, two crucial organelles for correct cell functioning.
“We have shown that the accumulation of dysfunctions in these two structures alters cell behavior and favors the appearance of pre-diabetes symptoms”, say the main authors of the article, David Sebastian and María Isabel Hernandez-Alvarez, post-doctoral fellows in Zorzano’s team.
The study has been published in Proceedings of the National Academy of Sciences (PNAS).