University of Hong Kong
A decline in metabolism and endurance of skeletal muscle is commonly observed in obese patients, but the underlying mechanism is not well-understood. A research team led by Dr Chi Bun CHAN, Assistant Professor from School of Biological Sciences, Faculty of Science, the University of Hong Kong (HKU), uncovers a new mechanism to explain how obesity jeopardizes the functions of skeletal muscle and provides a potential treatment against the disease. The research findings have recently been published in world-leading scientific journal Autophagy.
Obesity is a metabolic disorder with increasing prevalence in modern society. Since 1970s, the global number of obese people has trebled and reached 650 million (~ 13% of the total global population) in 2016. It is widely known that obesity provokes detrimental outcomes in multiple human organs and causes numerous chronic disorders such as diabetes, hypertension, fatty liver diseases, and atherosclerosis. Fat metabolism in the skeletal muscle of obese patients is slower than that of healthy people, which scientists believe is a consequence of abnormal functions in mitochondria (the powerhouses of a cell that convert nutrients into biological energy). However, how obesity impairs the activity of mitochondria is a long unresolved question.
To study the functional impacts of obesity on the skeletal muscle, Dr Chan’s team developed a special obesified mouse model by removing the gene of brain-derived neurotrophic factor (BDNF) exclusively in their skeletal muscle. BDNF is originally identified as an important growth factor for maintaining the survival and activities of neurons. Recent studies have proposed that BDNF is also a muscle-secreted protein (i.e., myokine), but its physiological significance is unknown.
For the first time, Dr Chan’s team found that obesity reduced the amount of BDNF in the skeletal muscle of mice. They also observed that the mice without BDNF in their muscle, called ‘MBKO‘ (Muscle-specific BDNF Knockout), gained more body weight and developed severer insulin resistance when the animals were fed with a high-fat diet. In addition, the research team found that MBKO mice have less energy expenditure than their control cohort.
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