Dubbed the powerhouses of the cell because
they turn nutrients into energy, mitochondria are tiny organelles that live
inside the cell and are key to metabolic health. New research offers fresh
insights into how they work and what keeps them healthy.
Because of the role of the mitochondria in metabolic and overall health,
previous research has suggested that dysfunction in these organelles may have
implications in conditions such as obesity and diabetes.
Other conditions that mitochondrial
dysfunction is involved in include age-related neurodegenerative conditions,
such as Parkinson’s, Alzheimer’s, and Huntington’s disease.
In fact, mitochondrial dysfunction may be at
the root of the aging process, in general. Although also disputed, the
so-called mitochondrial-free radical theory of aging is a popular one, and more
than one study has suggested that boosting mitochondria’s health
can prevent cells from aging.
But what exactly keeps mitochondria in tip-top
shape or makes them “unhealthy” remains unknown.
Previously, researchers thought that one
molecular pathway that they called autophagy might offer precious clues to what
keeps mitochondria healthy or makes them dysfunctional.
Autophagy — a word derived from ancient Greek
to mean “self-eating” — is a “cellular survival pathway that recycles intracellular
components to compensate for nutrient depletion and ensures the appropriate
degradation of organelles.”
Therefore, it is key for the health of
mitochondria, and previous studies have shown that exercise boosts autophagy,
and the researchers believed that a high fat diet might impair the process.
The latest research
looked at this pathway in mice and examined the ways in which exercise and a
high fat diet affect it, as well as how these changes affect mitochondrial
health.
Sarah Ehrlicher, a doctoral candidate in the
College of Public Health and Human Sciences at Oregon State University in
Corvallis, is the first author of the paper, which appears in the FASEB Journal.
Ehrlicher and colleagues “stressed” the
mitochondria of transgenic mice by making the animals exercise on a treadmill.
Genetic alterations impaired their exercise-induced autophagy pathway.
The rodents were euthanized 36 hours after
their last bout of exercise and 4 hours after their last meal, and the
researchers examined the mitochondria in the rodents’ muscle cells.
What the team found
was that despite the genetic modification and the added stress of exercise, the
mitochondrial function of the mice’s muscles remained intact.
As a next step, Ehrlicher and colleagues fed
the mice a high fat diet in addition to the exercise regimen to stress the
mitochondria even more.
Again, the mice’s mitochondria showed signs
of intact health and adaptation, even with the autophagy pathway blocked. This,
explains the study’s lead author, suggests that the mitochondria have
alternative ways to stimulate recycling and limit the damage.
Matt Robinson, a researcher in the same
department as Ehrlicher and the last and corresponding author of the study,
reports on the results.
He says, “[When]
these animals were given a high fat diet, they got better at burning off those
fats. If they were given just the exercise, they were able to make more
mitochondria, which is good from an exercise perspective. And
those adaptations seem to be very specific.”
The authors add that the findings elucidate
more about how mitochondria work and what keeps them healthy.
The study “helps lay some future groundwork
for how we can optimize (muscle and mitochondrial) health to promote their
health with diseases like obesity, diabetes, even some implications with aging
— conditions that we know have compromised mitochondria,” says Robinson.
Exercise may be one such way of optimizing
mitochondrial and metabolic health. “Even without changes in weight, exercise
has this amazing ability to improve metabolic health,” Ehrlicher says.
Obese mice do not seem to have an obvious
pathway dysfunction in their mitochondria, and the muscles just seem to respond
and adapt well to new stress, whether that is exercise or a high fat diet.
Source: Medical News Today
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