Madrid 24 cities. (European Press) –
Aerobic exercise not only trains your muscles, but it can also prevent the development of fatty liver. A new study by the German Center for Diabetes Research (DZD), Helmholtz in Munich and University Hospital Tübingen, shows observable molecular adaptations, particularly mitochondria in the liver, in this process, according to the authors in the journal Molecular Metabolism.
Worldwide, one in four people has nonalcoholic liver disease (NAFLD), also called metabolic liver disease. Those affected often have type 2 diabetes, as well as an increased risk of developing cirrhosis and cardiovascular disease.
Furthermore, NAFLD is associated with increased mortality. There is talk of an imbalance between energy intake and energy consumption as a cause of disease. This leads to the formation of fatty deposits in the liver and, over time, impairs mitochondrial function, both of which are risk factors for developing hepatic insulin resistance and hepatitis.
How exercise modifies the liver’s adaptation to increased energy intake To prevent and treat nonalcoholic fatty liver, it is recommended that you modify your lifestyle with increased physical activity.
Scientists from the Institute of Clinical Chemistry and Pathological Biochemistry of the University Hospital Tübingen and the Research Institute for Diabetes and Metabolic Diseases (IDM) of the Helmholtz Institute Munich of the University of Tübingen investigated the extent to which regular exercise modifies the liver’s increased energy consumption and what role skeletal muscle plays in this process, In collaboration with colleagues from the Institute for Experimental Genetics (IEG) in Helmholtz Munich, the Leibniz Institute for Analytical Sciences in Dortmund and the Institute of Chemical Physics in Dalian (China).
In the study, conducted by Dr. Miriam Howeney and Lisa Kapler, mice were fed a high-energy diet. Some also received regular treadmill training. After the six-week intervention, the researchers examined the animals’ liver and muscles for changes in transcriptome, mitochondrial protein, lipid composition, and mitochondrial function.
The results showed that training regulates important enzymes that break down glucose and fructose in the liver, as well as pyruvate metabolism in the mitochondria. Thus, substrate loading for mitochondrial respiration and lipid synthesis can be reduced.
As a result, less fat is stored in the liver and specific fats, such as diacylglycerol types, are reduced. In addition, glucose control is improved in exercise-trained mice. In addition, increasing the respiratory capacity of the skeletal muscles relieves the metabolic stress on the liver.
Systems Biology data provides a comprehensive view of the molecular adaptation of liver and muscle to high-energy diet, training, and combined effects.
“The results fit very well with approaches to ongoing clinical studies that test inhibitors against some of the targets found here, such as the mitochondrial pyruvate transporter,” highlights DZD scientist Dr. Cora Wiegert, study leader, and professor of molecular diabetes at the University Hospital Tübingen. “They also showed that regular physical activity simultaneously regulates many targets as key nodes in metabolic pathways, an effect that cannot be achieved with monotherapy.”
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