Obesity and muscle
How does obesity harm skeletal muscles and where is a possible cure?
Sergey Syrov, XX2 century
A decrease in the level of metabolism and skeletal muscle performance is a common problem of obese patients, but the mechanism of the phenomenon has been little studied. A research team led by Dr. Chi Bun Chan from the University of Hong Kong (HKU) explains how obesity harms skeletal muscle function. This explanation gives hope for the development of effective drugs.
An article about the study was published in the journal Autophagy (Ahuja et al., Muscle-generated BDNF (brain derived neurotrophic factor) maintains mitochondrial quality control in female mice)).
Obesity is a common metabolic disorder. Since the 1970s, the number of obese people in the world has tripled and by 2016 reached 650 million (approximately 13% of the total population of the planet). It is known that obesity has an extremely negative effect on organs and causes numerous chronic diseases: diabetes, hypertension, fatty liver diseases and atherosclerosis.
Fat metabolism in the skeletal muscles of obese patients is slower than in healthy people, which, according to experts, is a consequence of a malfunction of the mitochondria (the energy centers of the cell that convert nutrients into biological energy). The question of how obesity affects mitochondrial activity remains open.
To study the effect of obesity on skeletal muscles, Dr. Chang's team created an animal model of obesity — for this, the brain neurotrophic factor (BDNF) gene was removed from mice exclusively from their skeletal muscles. BDNF is an important growth factor for maintaining the vital activity and activity of neurons. But BDNF (and it was unclear why) is also secreted by muscles.
Initially, Dr. Chang's team found that obesity reduces the amount of BDNF in the skeletal muscles of mice. And mice without BDNF in the muscles (MBKO line — with the BDNF gene turned off, specific for muscles) are thicker than usual, and they have increased insulin resistance. In addition, MBKO mice are less active compared to the control cohort.
Biochemical, histological, metabolic and molecular analyses showed that mitochondria in the muscles of MBKO mice could not be processed normally — damaged mitochondria accumulated in the tissues. Because of this, lipid metabolism in the muscles of MBKO mice slows down noticeably, lipids accumulate, which affects insulin sensitivity.
BDNF is an important element in the process of mitophagy, the processing of spent mitochondria.
"It is obvious that muscle BDNF is a protein for weight control by increasing energy expenditure and maintaining insulin sensitivity," Dr. Chan summarizes. — BDNF has long been considered a peptide localized in the brain, and its importance in peripheral tissues has been underestimated. Our study provides a new insight into this area, and hopefully we can figure out the function of this myokine using our MBKO mice."
Is it possible to use new knowledge in obesity therapy? The research team tested whether restoring BDNF signals in muscles would help restore the mitochondrial disorder caused by obesity. Fat mice were fed 7,8-dihydroxyflavone (7,8-DHF), a naturally bioavailable mimetic of BDNF (found in the leaves of a South American plant Godmania aesculifolia, another reminder of the benefits of biodiversity conservation). This substance is undergoing clinical trials as a drug for Alzheimer's disease. It was found that the mitochondrial dysfunction caused by obesity is less pronounced with such therapy.
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