Some people lose weight more slowly than others after exercising, which raises a legitimate question: Why? A research team from Kobe University has found out.
It is well known that exercise burns fat, but for some people it is much harder to burn fat than for others, which raises doubts as to whether the mechanism behind losing or gaining weight is as simple as calories taken in exceeding calories burned.
Exercise responsive protein
Researchers have previously identified a protein called BGC-1 alpha that appears to link exercise and its effects. However, it has not been determined whether increasing the amount of this protein actually leads to the effects of exercise. The protein responds specifically to short-term exercise and controls the body’s energy expenditure.
The team studied what happens to mice that can’t produce the protein. These mice use less oxygen during exercise, burn less fat, and are more likely to gain weight. Since the team found that this link also exists in humans, the information they discover about this mechanism could provide a path to treating obesity.
Newly discovered copies
Recently, Wataru Ogawa, an endocrinologist at Kobe University, and other researchers found that there are actually several different versions of this protein.
According to the EurekAlert website, Ogawa explains that “these new versions of BGC-1 alpha, called “B” and “C,” have almost the same function as the traditional version “A,” but they are produced in the muscles more than ten times during exercise, while version “A” does not show this increase.
So the team demonstrated that the newly discovered versions – not the previously known ones – are what regulate energy expenditure during exercise.
To investigate, the researchers created mice that lacked the B and C versions of BGC1α, while still having the standard A version, and measured the mice’s muscle growth, fat burning and oxygen consumption during rest, short-term and long-term exercise.
They also invited people to participate in the test, both humans with and without type 2 diabetes, and subjected them to similar tests to the mice, because people with insulin intolerance and obesity are known to have low levels of the protein.
Do genes play a role?
Ogawa and his team found in their study, published in the journal Molecular Metabolism on June 23, that although all versions of the protein cause similar biological reactions, their different levels of production have far-reaching consequences for an organism’s health.
The lack of the alternative versions B and C of the BGC1 alpha protein means that the organism is essentially unable to respond to short-term activity and does not adapt to these stimuli, resulting in these individuals consuming less oxygen and burning less fat during and after exercise.
In humans, the research team found that the more individuals produced versions B and C of the protein, the more oxygen they consumed and the less body fat they had, whether they were healthy individuals or those with type 2 diabetes.
Ogawa summarizes these findings by saying: “Therefore, the hypothesis that genes in skeletal muscle determine susceptibility to obesity was correct.”
However, they also found that long-term exercise stimulates production of the standard “A” version of BGC-1 alpha, and that mice that exercised regularly over six weeks showed increased muscle mass regardless of whether they could produce the alternative versions of the protein.
A medicine that increases calorie burning
In addition to production in muscle, the Kobe University team looked at how production of different versions of BGC-1 alpha changed in fat tissue, and found no relevant effect in response to exercise.
However, given that animals also burn fat to maintain body temperature, the scientists looked at the ability of mice to tolerate cold. Indeed, they found that production of versions B and C of the BGC1 alpha protein in brown adipose tissue increased when the animals were exposed to cold, and that the body temperature of individuals who could not produce these versions decreased significantly under these conditions.
This may contribute to the increased body fat percentage of these individuals, but on the other hand it seems to suggest that versions B and C of the protein may be responsible for metabolic adaptations to short-term stimuli in general.
Ogawa and his team suggest that understanding the physiological activity of different versions of BGC1α could lead to treatments for obesity. Anti-obesity drugs have recently been developed that suppress appetite, but there are no drugs that treat obesity by increasing energy expenditure. If a substance that increases versions B and C is found, it could lead to the development of drugs that enhance energy expenditure during or even without exercise, and these drugs could treat obesity independently of dietary restrictions.
The team is now conducting research to learn more about the mechanisms that lead to increased production of protein B and C copies during exercise.