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7,8-Dihydroxyflavone–Restore Insulin Sensitivity

Many people know that obesity can easily lead to chronic diseases such as diabetes, hypertension, atherosclerosis, fatty liver, etc. In addition, the deterioration of muscle function is also a common phenomenon in obese patients.
Recently, the research team of the University of Hong Kong published a paper on the authoritative academic journal Autophagy, revealing the reasons why obesity leads to impaired skeletal muscle metabolism and decreased endurance. At the same time, they offer a potential treatment.

The research team found that obesity will cause skeletal muscle to reduce the secretion of a growth factor, which will slow down the speed of muscle fat metabolism. This growth factor is called brain-derived neurotrophic factor (BDNF). As the name implies, it is generally believed to originate from the brain and its function is to maintain the survival and activity of nerve cells. However, new research shows that BDNF is also a “muscle hormone”, and its function is related to weight control.

The team studied the role of BDNF secreted by muscle in obese mice and cultured cell models. They managed to remove the gene encoding BDNF from their skeletal muscle in experimental mice. After the mice with this gene defect ate high-fat food, they were not only more likely to get fat, but also had more severe insulin resistance. Compared with control mice, the energy consumption of mice whose muscles could not normally secrete BDNF was significantly lower.

A series of biochemical, histological, and metabonomic experiments showed that this was because the lack of BDNF in muscle cells would cause problems in mitochondrial turnover.

The important function of mitochondria is to use nutrients to produce energy for cells. When they are normally consumed, they can be recovered and cleared through a process called autophagy. However, the absence of BDNF prevented its downstream signal pathway from starting, and damaged mitochondria changed from recyclable garbage to non recyclable garbage, accumulating in muscle tissue. As a result, the ability of muscle to metabolize fat decreases, resulting in the deposition of a lot of fat in muscle cells, which interferes with the muscle’s sensitivity to insulin.

It can be seen that muscle BDNF is a kind of weight control protein, which plays a role by increasing energy consumption and maintaining insulin sensitivity.” Dr. Chen Zhibin, who led the study, concluded.

Next, the research team tried to translate the above findings into therapeutic applications: can boosting BDNF signals for obese animals help muscles restore metabolic capacity?

The researchers fed obese mice an oral drug called 7,8-dihydroxyflavone (7,8-DHF). This is the first natural flavonoid molecule found in the leaves of South American plants, which can simulate BDNF to enhance its downstream signal, and is currently used in clinical research on the treatment of Alzheimer’s disease.

The researchers found that after three months of oral treatment with 7,8-dihydroxyflavone, the number of damaged mitochondria in the muscle of obese mice was significantly reduced.

It is worth noting that Dr. Chen Zhibin and his colleagues also found in previous studies that oral administration of 7,8-dihydroxyflavone can help female obese mice lose weight and restore insulin sensitivity. Therefore, combined with this series of research results, it not only provides us with a new understanding of why obesity damages muscles, but also further demonstrates that therapeutic strategies to enhance BDNF signals have potential to be used in the treatment of human obesity in the future.

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