Mitochondria are responsible for creating energy, which fuels cells and keeps them functioning. However, mitochondrial abnormalities have been linked to the development of disorders like type 2 diabetes. Patients with this illness are unable to produce enough insulin or use the insulin produced by their pancreas to maintain normal blood sugar levels.
Mitochondria are responsible for creating
energy, which fuels cells and keeps them functioning. However, mitochondrial
abnormalities have been linked to the development of disorders like type 2
diabetes. Patients with this illness are unable to produce enough insulin or
use the insulin produced by their pancreas to maintain normal blood sugar
levels.
Researchers
at the University of Michigan used mice to show that dysfunctional mitochondria
trigger a response that affects the maturation and function of b-cells.
Several studies have shown that insulin-producing pancreatic b-cells of
patients with diabetes have abnormal mitochondria and are unable to generate
energy. Yet, these studies were unable to explain why the cells behaved this
way.
"We wanted to
determine which pathways are important for maintaining the proper mitochondrial
function," said Emily M. Walker, Ph.D, a research assistant professor of
internal medicine and first author of the study.
To do so,
the team damaged three components that are essential for mitochondrial
function: their DNA, a pathway used to get rid of damaged mitochondria, and one
that maintains a healthy pool of mitochondria in the cell.
"In all three cases, the exact same
stress response was turned on, which caused b-cells to become immature, stop
making enough insulin, and essentially stop being b-cells," Walker said.
"Our results demonstrate that the mitochondria can send signals to the
nucleus and change the fate of the cell."
The
researchers also confirmed their findings in human pancreatic islet cells.
Their results prompted the team to expand their search into other cells that
are affected by diabetes.
Losing
your b-cells is the most direct path to getting type 2 diabetes. Through our
study we now have an explanation for what might be happening and how we can
intervene and fix the root cause," said Scott A. Soleimanpour, M.D.
"Diabetes
is a multi-system disease--you gain weight, your liver produces too much sugar
and your muscles are affected. That's why we wanted to look at other tissues as
well," said Scott A. Soleimanpour, M.D., director of the Michigan Diabetes
Research Center and senior author of the study.
The team
repeated their mouse experiments in liver cells and fat-storing cells and saw
that the same stress response was turned on. Both cell types were unable to
mature and function properly.
"Although
we haven't tested all possible cell types, we believe that our results could be
applicable to all the different tissues that are affected by diabetes,"
Soleimanpour said.
Regardless
of the cell type, the researchers found that damage to the mitochondria did not
cause cell death.
This
observation brought up the possibility that if they could reverse the damage,
the cells would function normally.
To do so,
they used a drug called ISRIB that blocked the stress response. They found that
after four weeks, the b-cells regained their ability to control glucose levels
in mice.
"Losing
your b-cells is the most direct path to getting type 2 diabetes. Through our
study we now have an explanation for what might be happening and how we can
intervene and fix the root cause," Soleimanpour said.
The team
is working on further dissecting the cellular pathways that are disrupted and hopes
that they will be able to replicate their results in cell samples from diabetic
patients. (ANI)
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