Insulin resistance is characterized by the lack of tissue response to insulin and is counteracted by a greater production of insulin by the pancreas. When the pancreas does not have the capacity to produce the amount of insulin required for tissues to receive glucose, glucose in blood increases to pathological levels and the individual goes from being insulin-resistant to suffering type 2 diabetes.
Although it is unclear what makes people develop insulin resistance, several studies report that resistant subjects show functional alterations in mitochondria. These intracellular organelles are responsible for transforming glucose into energy that the cell will then use to perform several functions. A study performed by the researcher Marc Liesa, a member of Antoni Zorzano’s lab at the Institute for Research in Biomedicine (IRB Barcelona), describes a new control pathway of a gene responsible for mitochrondrial fusion, a process that contributes to the correct function of these organelles. This pathway could therefore be a key component in the development of insulin resistance. The results of this study have been published in the scientific journal PloS One.
Diabetes: a complex genetic map
Previous studies demonstrated that people resistant to insulin have altered mitochondrial capacity to “generate” energy through a process called oxidative phosphorylation. In a study performed in 2003, two possible main actors were identified, the genes PGC1-beta and PGC1-alpha. These two genes are responsible for regulating the whole cascade of genes and proteins that allow mitochondria to produce energy by means of oxidative phosphorylation. Now, for the first time, 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 therapeutic target of interest”, concludes Zorzano.
Type 2 diabetes currently affects 6.5% of the populated aged between 30 and 65 in Spain and recent years have witnessed an increasing incidence of this disease among adolescents and children.
Sònia Armengou | alfa
Small but versatile; key players in the marine nitrogen cycle can utilize cyanate and urea
10.12.2018 | Max-Planck-Institut für Marine Mikrobiologie
Carnegie Mellon researchers probe hydrogen bonds using new technique
10.12.2018 | Carnegie Mellon University
What if a sensor sensing a thing could be part of the thing itself? Rice University engineers believe they have a two-dimensional solution to do just that.
Rice engineers led by materials scientists Pulickel Ajayan and Jun Lou have developed a method to make atom-flat sensors that seamlessly integrate with devices...
Scientists at the University of Stuttgart and the Karlsruhe Institute of Technology (KIT) succeed in important further development on the way to quantum Computers.
Quantum computers one day should be able to solve certain computing problems much faster than a classical computer. One of the most promising approaches is...
New Project SNAPSTER: Novel luminescent materials by encapsulating phosphorescent metal clusters with organic liquid crystals
Nowadays energy conversion in lighting and optoelectronic devices requires the use of rare earth oxides.
Scientists have discovered the first synthetic material that becomes thicker - at the molecular level - as it is stretched.
Researchers led by Dr Devesh Mistry from the University of Leeds discovered a new non-porous material that has unique and inherent "auxetic" stretching...
Scientists from the Theory Department of the Max Planck Institute for the Structure and Dynamics of Matter (MPSD) at the Center for Free-Electron Laser Science (CFEL) in Hamburg have shown through theoretical calculations and computer simulations that the force between electrons and lattice distortions in an atomically thin two-dimensional superconductor can be controlled with virtual photons. This could aid the development of new superconductors for energy-saving devices and many other technical applications.
The vacuum is not empty. It may sound like magic to laypeople but it has occupied physicists since the birth of quantum mechanics.
10.12.2018 | Event News
06.12.2018 | Event News
03.12.2018 | Event News
10.12.2018 | Life Sciences
10.12.2018 | Physics and Astronomy
10.12.2018 | Life Sciences