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Researchers at IRB Barcelona validate the potential of a protein for the treatment of type 2 diabetes

By 23 de March de 2012November 18th, 2020No Comments
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Researchers at IRB Barcelona validate the potential of a protein for the treatment of type 2 diabetes

Investigadors de l'Institut de Recerca Biomèdica (IRB Barcelona) –amb seu al Parc Científic Barcelona– han descobert que la deficiència d'una única proteïna, Mitofusina 2, en les cèl·lules del múscul i del fetge en ratolins és suficient per provocar que els teixits es tornin insensibles a la insulina amb el consegüent augment de glucosa en sang. Aquestes són les dues condicions habituals prèvies al desenvolupament d'una diabetis tipus 2. L'estudi, publicat aquesta setmana al Proceedings of the National Academy of Sciences (PNAS), valida la Mitofusina 2 com una possible diana per al tractament de la diabetis de tipus 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.

The World Health Organization estimates that there will be 350 million people suffering from diabetes in 2020. Diabetes type 2 accounts for 90% of diabetes cases and is due to a great extent to excess body weight, poor nutrition and sedentary lifestyle. According to the Spanish Society of Diabetes, in Spain 6.5% of the current population between 30 and 65 years has this disease and about 11.6 % of Spaniards are at risk of developing it.

Target: Mitofusin 2

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 signaling 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 Sebastián and María Isabel Hernández-Álvarez, post-doctoral fellows in Zorzano’s team.

The study has been partially funded by the European projects MITIN, part of the Seventh Framework Programme (FP7), and DIOMED, belonging to INTERREG/SUDOE/FEDER, both coordinated by Antonio Zorzano at IRB Barcelona, with the support of the “CIBER de Diabetes y Enfermedades Metabólicas Asociadas” (CIBERDEM), of the “Instituto de Salud Carlos III”.

Reference article: David Sebastián, María Isabel Hernández-Alvarez, Jessica Segalés, Eleonora Sorianello, Juan Pablo Muñoz, David Sala, Aurélie Waget, Marc Liesa, José C. Paz, Gopal Peddinti, Matej Orešič, Sara Pich, Remy Burcelin, Manuel Palacín, Antonio Zorzano.Mitofusin 2 (Mfn2) links mitochondrial and endoplasmic reticulum function with insulin signaling and is essential for normal glucose homeostasis. PNAS 2012 [published ahead of print] March 16, 2012, doi:10.1073/pnas.1108220109.

Imatge: Hepatic cells isolated from healthy mice and mice deficient in Mitofusin 2. Morphology of mitochondria (red), more rounded, is altered in the image on the right.