Diabetes: New pathway to treatment suggested by protein culprit
Gastric band Surgery In France Diabetes: New pathway to treatment suggested by protein culprit What is the link between anxiety and diabetes? New research shows that a protein related to the development of anxiety and depression may also play a role in triggering diabetes. Scientists from the Max Planck Institutes hypothesize that an antagonist compound could be used to block its effect. Scientists investigate a new lead in the search for better diabetes treatments. The main known causes for type 2 diabetes so far include obesity and lack of physical exercise – both of which can lead to insulin resistance – as well as a family history of the condition. Insulin resistance occurs when muscles, liver, and fat cells become unable to use insulin appropriately, which ultimately leads to a dangerous rise in blood glucose levels. Now, researchers from the Max Planck Institute of Psychiatry in Munich, Germany, have found that a protein called FKBP51 may also play a role in triggering type 2 diabetes. The protein has so far been associated with anxiety and depression; it contributes to the regulation of the stress system. When the gene that controls the production of FKBP51 suffers a mutation, this can lead to dysregulation of the stress system, which, in turn, can cause mental health disorders. Mathias Schmidt – lead researcher of the current study – and colleagues have recently noted that the FKBP51 protein also contributes to forming a molecular link between the stress system and the regulation of various metabolic functions. This may make FKBP51 responsible for the onset of metabolic diseases such as obesity and diabetes. The team’s findings have now been published in the journal Nature Communications. Protein reacts to metabolic stress Schmidt and team looked at a mouse model to understand the potential role played by FKBP51 in metabolic processes. They studied the effect of a high-fat diet on mice in which the FKBP51 gene was expressed, as well as on knockout mice, in which that gene was inactivated artificially. They found that the knockout mice did not gain weight after exposure to the diet, had better glucose, or blood sugar, tolerance, and had more effective insulin signaling. This allowed the researchers to understand that the FKBP51 protein – regulated by the gene with the same name – affects signaling pathways in skeletal muscles. Since the protein is sensitive to metabolic stress factors, such as high fat intake, it can ultimately lead to blood sugar buildup and insulin resistance. These are the main factors to blame in the development of type 2 diabetes and obesity. “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 The cause may lead to the treatment Fortunately, this mechanism has also offered the scientists an insight into how they might be able to prevent FKBP51’s response to the
