Researchers at IRB Barcelona produce more data on key genes i...(me a study has shown that another gene c...)

Date:11/19/2008

me, a study has shown that another gene, called Mitofusin 2 (Mfn2), which is decreased in diabetic patients, is also controlled by PGC1-beta. This information is highly relevant because until now it was considered that PGC1-beta controlled the production of energy only by regulating the expression of mitochondrial genes responsible for oxidative phosphorylation. "We have discovered what the cell does to regulate this mitochondrial fusion gene and we explain why this gene is decreased in diabetes, as it is regulated by PGC1-beta, which in turn is affected by this disease. However, although this evidence allows us to propose interesting hypotheses as to the role of Mfn2, its exact role remains unknown", explains the first author of the study, Marc Liesa.

Key or secondary role in diabetes?

One of the hypotheses is that mitochondrial fusion is crucial for the correct function of these organelles and when the gene that regulates this fusion is decreased, the function of mitochondria is also impaired. But where is Mfn2 situated in the genetic map of diabetes? Is the decrease in mitochondrial fusion related directly to the appearance of insulin resistance? The researchers have obtained the first data that support the notion that Mfn2 plays a key role.

In 2005, in experiments in vitro using rat skeletal muscle cells, the scientists removed the expression of only the Mfn2 gene without touching PGC1-beta, and confirmed that the decrease in mitochondrial fusion affected the capacity to generate energy, "regardless of whether PGC1-beta is functioning correctly", stresses the head of the group, Antonio Zorzano. "What we are proposing is that the alteration in the fusion alters mitochondrial activity. Observation that the removal of only Mfn2 produces insulin resistance in later experiments in a simple living model not only in individual cells - , would imply that modulation of this gene contributes to this pathology, thereby making Mfn2 a the
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Contact: Sonia Armengou sonia.armengou@irbbarcelona.org 34-934-037-255 Institute for Research in Biomedicine (IRB Barcelona) Source:Eurekalert

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