And Sugar Overload
Excess fat and sugar don't just pack on the pounds but also cause
severe metabolic stress and can push some cells in the body to commit suicide. These cells don't have the ability to tolerate the toxic environment excess fat and sugar cause, and ultimately initiate their own death.
severe metabolic stress and can push some cells in the body to commit suicide. These cells don't have the ability to tolerate the toxic environment excess fat and sugar cause, and ultimately initiate their own death.
Research scientists at Washington University School of Medicine in
St. Louis have recently discovered three unexpected culprits that help
a cell overloaded with fat commit suicide. They've demonstrated that
these molecules leading a cell to self-destruct are small strands of RNA,
not proteins. Since these small nuclear RNAs play well-known roles
in building proteins, the researchers were surprised to discover them
killing cells.
St. Louis have recently discovered three unexpected culprits that help
a cell overloaded with fat commit suicide. They've demonstrated that
these molecules leading a cell to self-destruct are small strands of RNA,
not proteins. Since these small nuclear RNAs play well-known roles
in building proteins, the researchers were surprised to discover them
killing cells.
The research has been published in Cell Metabolism. It is the first study
to link these small RNA molecules to the cellular damage characteristic
of common metabolic diseases like diabetes.
to link these small RNA molecules to the cellular damage characteristic
of common metabolic diseases like diabetes.
"When these three RNAs are present, the cells die in response to
metabolic stress, such as exposure to large amounts of fats," says cardiologist Jean E. Schaffer, MD, the Virginia Minnich Distinguished Professor of Medicine at Washington University. "But if these three
RNAs are missing, the cells don't die."
metabolic stress, such as exposure to large amounts of fats," says cardiologist Jean E. Schaffer, MD, the Virginia Minnich Distinguished Professor of Medicine at Washington University. "But if these three
RNAs are missing, the cells don't die."
It's important to recognize that cell suicide is a natural process that protects healthy tissues from damaged cells, but the process can sometimes fall out of balance. For example, if the cell death pathway
gets shut down, damaged cells may
divide and lead to cancer.
gets shut down, damaged cells may
divide and lead to cancer.
Conversely, too much cell death due to abnormal metabolites, such as high levels of fats and sugar, can impair the function of tissues in the body. This type of excess cell death is involved with
diabetes complications such as heart failure. It is important to
understand how abnormal metabolites cause cells to die, it will be
helpful in the search for effective new therapies.
diabetes complications such as heart failure. It is important to
understand how abnormal metabolites cause cells to die, it will be
helpful in the search for effective new therapies.
According to Dr.Schaffer, who is also the director of the Diabetic Cardiovascular Disease Center and Diabetes Research Training
Center at the School of Medicine, the fact that small RNA molecules
are involved in this cell death pathway is totally unexpected.
Center at the School of Medicine, the fact that small RNA molecules
are involved in this cell death pathway is totally unexpected.
"When we set out to find genes causing cellular damage due to excess
fat, we were expecting to find genes that code for proteins," she explains. "Instead, we identified an entirely new function for three small nuclear RNAs. Unrelated to their well-defined role in the cell's protein-making machinery, we discovered they participate in how cells go on to die
from overload of nutrients."
fat, we were expecting to find genes that code for proteins," she explains. "Instead, we identified an entirely new function for three small nuclear RNAs. Unrelated to their well-defined role in the cell's protein-making machinery, we discovered they participate in how cells go on to die
from overload of nutrients."
In a classic genetics experiment, the researchers initially identified a genetic region that, when disabled, allows cells to continue living in high
fat and high sugar conditions. While the region codes for a protein, they demonstrated that the protein itself is not involved in initiating cell death.
fat and high sugar conditions. While the region codes for a protein, they demonstrated that the protein itself is not involved in initiating cell death.
"At first this result really puzzled us," Dr. Schaffer continued. "The
mutation occurs in a region that encodes a protein, as we might expect.
But returning the protein to the mutated cells did not return the cell death response."
The three small nuclear RNAs function together not only to promote
cell death from nutrient excess, but also to promote more general mechanisms of cell death in diseased tissues.
mutation occurs in a region that encodes a protein, as we might expect.
But returning the protein to the mutated cells did not return the cell death response."
The three small nuclear RNAs function together not only to promote
cell death from nutrient excess, but also to promote more general mechanisms of cell death in diseased tissues.
As a cardiologist who treats patients at Barnes-Jewish Hospital, Dr. Schaffer explains how a multifaceted approach is necessary to manage
the complexities of metabolic diseases like diabetes and obesity. Encouraging patients to reduce the amount of fat and sugar in the diet
is a key strategy for treatment.
the complexities of metabolic diseases like diabetes and obesity. Encouraging patients to reduce the amount of fat and sugar in the diet
is a key strategy for treatment.
When dieatry modification becomes ineffective, it would be helpful to
have other ways to reduce cellular damage from excess fats in the
muscles, heart, pancreas, liver and other organs and the team continues
to pursue the search for possible treatments. "That's where our future
work is headed."
have other ways to reduce cellular damage from excess fats in the
muscles, heart, pancreas, liver and other organs and the team continues
to pursue the search for possible treatments. "That's where our future
work is headed."
This research was supported by grants from the National Institutes of
Health (NIH), the Burroughs Wellcome Foundation, the Washington University Diabetes Research Training Center and the Washington University Metabolomics facility.
Health (NIH), the Burroughs Wellcome Foundation, the Washington University Diabetes Research Training Center and the Washington University Metabolomics facility.
Story Source: Washington University School of Medicine.
Journal Reference: Small nuclear RNAs U32a, U33 and U35a
are critical mediators of metabolic stress. Cell Metabolism, July 2011
are critical mediators of metabolic stress. Cell Metabolism, July 2011
This article is for informational and educational purposes only, and is not intended to provide medical advice, diagnosis or treatment. Contact your doctor or healthcare professional for medical and nutritional consultation.
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