Doctors always remind people that exercise can help prevent many diseases, including heart disease, Alzheimer's disease, diabetes and infection. However, the biological and molecular basis of exercise for health has not been clear for a long time.
Recently, researchers from the University of Texas Southwestern Medical Center obtained some clues to solve this puzzle. They confirmed that the wonderful effect of exercise is to promote autophagy. The relevant research results were published online in the journal Nature on January 18. Beth Levine, head of the autophagy research department at the University of Texas Southwestern Medical Center and professor of internal medicine and microbiology, led the research. She has made a large number of important research findings in the field of autophagy. In 1999, she discovered Beclin1, the first mammalian autophagy gene related to breast cancer suppressor, which is the first autophagy gene related to human genes discovered by scientists.
Autophagy was proposed by Ashford and Porter after they discovered the phenomenon of "eating yourself" in autophagy in 1962. It refers to that part of the cytoplasm and organelles, proteins and other components in the cell that need to be degraded are wrapped by the double-layer membrane falling off the ribosome free attachment area of the rough endoplasmic reticulum to form autophagosome, which is fused with lysosomes to form autophagosomes and degrade the contents, It is a catabolic process to realize the metabolic needs of the cell itself and the renewal of some organelles.
As an evolutionarily very ancient and conservative metabolic pathway, autophagy is involved in regulating the metabolic balance between the synthesis, degradation and reuse of cellular substances, and affects all aspects of biological life processes. Then the researchers put the normal and transgenic mice on the treadmill for half an hour. They found that the transgenic mice showed early exhaustion compared with the normal mice. This is because mutant mice can not improve autophagy, resulting in abnormal glucose metabolism, so they can not generate enough energy.
In the next high-fat diet experiment, the researchers verified the results again. They found that in the absence of exercise, wild-type mice and transgenic mice given a high-fat diet significantly increased their weight and developed diseases similar to type 2 diabetes. However, under normal exercise, the researchers found that although exercise reduced the weight of the two groups of mice, the blood glucose levels of the mutant mice were still high. Manipulation of autophagy may be a new approach to the treatment of diabetes. The research team also plans to further analyze the role of autophagy in exercise prevention of other diseases, including cancer, neurodegenerative diseases and aging in the next stage of experimental research.
