Effect of fat supplemented diets and deficient nicotinamide nucleotide transhydrogenase on oxidative stress levels in C. elegans
Document Type
Oral Presentation
Campus where you would like to present
SURC Ballroom A
Start Date
17-5-2012
End Date
17-5-2012
Abstract
In 2010, the Centers for Disease Control and Prevention reported that in the United States, diabetes affects 25.8 million people or 8.3% of the population. Diabetes is, in fact, the most prevalent metabolic disorder in the world, though the cellular mechanisms which initiate the disease are still unclear. Recent research indicates that there may be a link between mitochondrial dysfunction and type 2 diabetes. The aim of this work was to investigate the role of a mitochondrial enzyme, Nicotinamide Nucleotide Transhydrogenase (NNT-1), in maintaining mitochondrial function in Caenorhabditis elegans exposed to fat supplemented diets including stearic or oleic fatty acids. The nnt-1 mutant worms lack functional NNT-1 protein in their mitochondria. These worms are highly susceptible to free radical oxidation as NNT-1 produces NADPH, which is used for free radical detoxification. In this study, the chronic effect of fat supplemented diets and deficient NNT-1 status was investigated in two strains of C. elegans, including the wild-type (N2) worm and an nnt-1 mutant. The scope of this research includes observing mitochondrial function through oxygen consumption and ATP measurements, and lipid peroxidation levels through measurements of the oxidized lipid breakdown product malondialdehyde (MDA). Preliminary data suggests that the nnt-1 mutant worms undergo more oxidative stress as seen in their elevated MDA content as compared to wild-type worms. Additionally, the mutant worms exposed to fat supplemented diets have lower ATP levels, suggesting dysfunctional mitochondrial oxidative phosphorylation. This is in contrast to the oxygen consumption studies, where no difference was observed.
Recommended Citation
Carter, John, "Effect of fat supplemented diets and deficient nicotinamide nucleotide transhydrogenase on oxidative stress levels in C. elegans" (2012). Symposium Of University Research and Creative Expression (SOURCE). 22.
https://digitalcommons.cwu.edu/source/2012/posters/22
Poster Number
30
Additional Mentoring Department
Chemistry
Additional Mentoring Department
Biological Sciences
Effect of fat supplemented diets and deficient nicotinamide nucleotide transhydrogenase on oxidative stress levels in C. elegans
SURC Ballroom A
In 2010, the Centers for Disease Control and Prevention reported that in the United States, diabetes affects 25.8 million people or 8.3% of the population. Diabetes is, in fact, the most prevalent metabolic disorder in the world, though the cellular mechanisms which initiate the disease are still unclear. Recent research indicates that there may be a link between mitochondrial dysfunction and type 2 diabetes. The aim of this work was to investigate the role of a mitochondrial enzyme, Nicotinamide Nucleotide Transhydrogenase (NNT-1), in maintaining mitochondrial function in Caenorhabditis elegans exposed to fat supplemented diets including stearic or oleic fatty acids. The nnt-1 mutant worms lack functional NNT-1 protein in their mitochondria. These worms are highly susceptible to free radical oxidation as NNT-1 produces NADPH, which is used for free radical detoxification. In this study, the chronic effect of fat supplemented diets and deficient NNT-1 status was investigated in two strains of C. elegans, including the wild-type (N2) worm and an nnt-1 mutant. The scope of this research includes observing mitochondrial function through oxygen consumption and ATP measurements, and lipid peroxidation levels through measurements of the oxidized lipid breakdown product malondialdehyde (MDA). Preliminary data suggests that the nnt-1 mutant worms undergo more oxidative stress as seen in their elevated MDA content as compared to wild-type worms. Additionally, the mutant worms exposed to fat supplemented diets have lower ATP levels, suggesting dysfunctional mitochondrial oxidative phosphorylation. This is in contrast to the oxygen consumption studies, where no difference was observed.
Faculty Mentor(s)
Carin Thomas, Lucinda Carnell