Geschatte leestijd: 2 minutenGerman researchers have shown that a “stress protein” in muscles increases the risk of diabetes. Disabling the function of this protein may offer a new treatment method.
Stress Protein
Researchers from the Max Planck Institute in Munich have demonstrated that a “stress protein” in muscles increases the risk of glucose intolerance and thereby the risk of diabetes. This insight offers the possibility of new treatment methods for both conditions.
It has been known for some time that (increased expression of the gene for) the protein called FKBP51 is associated with depression and anxiety disorders. It plays a role in the regulation of the stress system and is influenced, among other things, by diet. When this system does not function properly, mental problems can arise. However, researchers at the Max Planck Institute have discovered a new and surprising role for this protein. FK506-binding 51 protein, or FKBP51, is a protein that acts as a molecular link between the stress regulatory system and metabolic processes. It is mainly found in muscle tissue and fat tissue.
FKBP51 influences a signaling cascade in muscle tissue, which with excessive calorie intake leads to the development of glucose intolerance, i.e., the key indicator of diabetes type 2,
Mathias Schmidt
An unhealthy diet high in fats can cause a stress reaction in the body. This can lead to an increased production of FKBP15 in the muscles. This increase in this stress protein now also appears to result in reduced glucose uptake by the muscles. This glucose intolerance is a precursor to both diabetes and obesity.
“Blocking stress protein prevents diabetes”
In the study, genetically blocking the FKBP15 protein in mice prevented diabetes from developing, even when overeating occurred. Disabling the FKBP15 gene meant normal glucose tolerance, increased insulin sensitivity, and thus normal metabolism. Moreover, the weight gain from the excess calories was prevented.
This blocking can also be achieved with medication using substances developed by Felix Hausch at the Max Planck Institute. Chronic use of this antagonist, called SAFit2, showed the same effect as genetically disabling FKBP15 in mice on weight and glucose tolerance. Shorter use of SAFit2 showed that improved glucose tolerance precedes the lowering effect on body weight.
The institute’s director, Alon Chen, believes that the discoveries could lead to an entirely new treatment method for diabetes.
We’ve certainly heard that before.
References
- Georgia Balsevich, Alexander S. Häusl, Carola W. Meyer, Stoyo Karamihalev, Xixi Feng, Max L. Pöhlmann, Carine Dournes, Andres Uribe-Marino, Sara Santarelli, Christiana Labermaier, Kathrin Hafner, Tianqi Mao, Michaela Breitsamer, Marily Theodoropoulou, Christian Namendorf, Manfred Uhr, Marcelo Paez-Pereda, Gerhard Winter, Felix Hausch, Alon Chen, Matthias H. Tschöp, Theo Rein, Nils C. Gassen, Mathias V. Schmidt. Stress-responsive FKBP51 regulates AKT2-AS160 signaling and metabolic function. Nature Communications, 2017; 8 (1) DOI: 10.1038/s41467-017-01783-y
