A new study shows how obesity damages the metabolism and endurance of muscle. It was already well known that being obese leads to reduced muscular function, but the precise mechanism was unclear.
This new study is yet more evidence – as if more evidence were needed – that being seriously overweight is terrible for you.
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Obesity damages muscle function: new study
Since the 1970s, the global number of obese people has trebled. In 2016, there were 650 million obese people in the world – 13% of the total global population.
It hardly needs saying that obesity is linked with a whole range of detrimental outcomes, chronic disorders and diseases, including diabetes, hypertension, fatty liver diseases, and atherosclerosis.
One consequence of obesity is that fat metabolism in the skeletal muscle becomes slower than that of healthy people. Scientists believe this 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, a group of researchers led by Dr Chi Bun CHAN, Assistant Professor from School of Biological Sciences, Faculty of Science, the University of Hong Kong (HKU) began by developing a special obesified mouse model.
They did this by removing the gene for brain-derived neurotrophic factor (BDNF) from the skeletal muscle of the mice. BDNF was originally identified as an important growth factor for maintaining the survival and activities of neurons, and more recent research has suggested that BDNF is also a muscle-secreted protein (i.e., myokine). At present, its physiological significance is unknown.
Dr Chan’s team discovered 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 far worse insulin resistance when the animals were fed a high-fat diet. In addition, the MBKO mice expended less energy than their control cohort.
By applying a variety of complex analyses, the researchers further demonstrated that the mitochondria in the muscle of the MBKO mice could not be recycled, leading to the accumulation of damaged mitochondria in the tissues. Consequently, the lipid metabolism in the muscle of MBKO mice was retarded, lipids to accumulate and interfere with insulin sensitivity.
Ubiquitous pesticide may be helping to cause worldwide obesity explosion
A recent study from McMaster University, in Canada, suggests that chlorpyrifos, a commonly used pesticide, may be responsible for obesity. Researchers observed that the pesticide causes the brown fat tissue of mice to burn calories at a reduced rate, promoting fat storage. Even small changes to the metabolic rate of this tissue can, in the long term, trigger significant weight gain.
Although chlorpyrifos is banned in Canada, where the study was carried out, it is widely used around the world to treat fruit and vegetable crops. According to its former manufacturer Dow (now part of Corteva after a merger), in 2014 chlorpyrifos was used in 100 countries around the world and sprayed on 8.5 million acres of crops.
Chlorpyrifos is already in the news due to a massive class-action lawsuit in the United States which alleges that the pesticide caused brain damage to children in a heavily sprayed area of California.
CLICK HERE TO READ MORE ABOUT THIS NASTY SUBSTANCE AND ITS NASTY EFFECTS
“Clearly, muscle-derived BDNF is a weight-control protein by increasing the energy expenditure and maintaining insulin sensitivity,” said Dr Chan.
“BDNF has long been considered a brain-localized peptide, and its importance in peripheral tissues has been underestimated. Our study provides a new insight to this area, and hopefully we can unlock more functions of this myokine using our MBKO mice,” Dr Chan further added.
The team also used cultured cell models to discover the molecular mechanism behind the changes in BDNF-deficient muscle cells. They found that muscle-secreted BDNF used AMPK-activated protein kinase, the well-known energy sensor in cells, to trigger the Parkin/PINK1 pathway for inducing mitophagy (a mechanism to recycle the materials in cells) in skeletal muscle.
In order to begin investigating possible therapeutic applications of their findings, the researchers tested if restoring the BDNF signaling in muscle would rescue the obesity-induced mitochondrial damage.
To do this they fed the obese mice with 7,8-dihydroxyflavone, a natural plant compound that mimics BDNF (found in the leaves of Godmania aesculifolia, a plant species in South America) and is currently being used in clinical trials for Alzheimer’s disease. The team found that, yes, the mitochondrial dysfunction was reduced.
The team’s work provides a new explanation for the pernicious nature of obesity – just how it becomes a “vicious cycle” which is so hard to escape – and suggests that BDNF-signaling enhancers such as 7,8-DHF could be used in the future to treat obesity in human beings.
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