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050 4 a| RB147b| .W66 2005;

100 1 a| Woodlief, Tracey L.,e| author.?| UNAUTHORIZED;

245 10 a| Peroxisomal enhancement of mitochondrial function /c| by Tracey L. Woodlief.;

264 0 c| 2005.;

300 a| 99 leaves :b| illustrations ;c| 28 cm;

336 a| textb| txt2| rdacontent;

337 a| unmediatedb| n2| rdamedia;

338 a| volumeb| nc2| rdacarrier;

502 b| M.S.c| East Carolina Universityd| 2005;

500 a| Presented to the faculty of the Department of Biology.;

500 a| Advisor: Ronald N. Cortright;

520 3 a| Background: Lipid disposal pathways have been shown to be dysregulated in disease states such as obesity and diabetes, with a main focus of research being on mitochondrial dysfunction. More so, little data exists on peroxisomal function in skeletal muscle, the major tissue responsible for lipid disposal in the healthy or diseased state. Accordingly, it has been hypothesized that mitochondrial impairments in fatty acid oxidation may be compensated for by peroxisomal metabolism of fatty acids to acylcarnintines which can bypass mitochondrial transport mechanisms and enhance efficiency. Purpose: To test the direct effects elevated peroxisomal content on skeletal muscle mitochondrial function. Methods: Peroxisomes and mitochondria I were isolated from rat liver and whole gastrocnemius, respectively, using an Optiprep density gradient system. Oxidation rates (as captured 14CO2 and acid soluble metabolites) were compared via peroxisomal titration experiments under the following conditions: 1) mitochondria plus 1-14C Palmitic Acid (long-chain fatty acid; LCFA) ± malonyl-CoA ± peroxisomes 2) mitochondria plus 1-14C lignoceric acid (very long-chain fatty acid; VLCFA) ± malonyl-CoA ± increasing peroxisomal content. Results: Skeletal muscle mitochondrial oxidation of VLCFA was linearly enhanced in the presence of increasing peroxisomal content. Mitochondrial oxidation of LCFA was not enhanced in the basal state (- malonyl-CoA); however, oxidation of LCFA was increased in the presence of malonyl-CoA, suggesting that peroxisomes represent an alternative pathway for oxidizing LCFA in the disease state characterized by dysfunctional mitochondria. Conclusion: This study is the first to directly demonstrate that increasing peroxisomal content results in increased mitochondrial oxidation of fatty acids, suggesting a viable metabolic target for therapeutic intervention that could lower intramuscular lipids suspected to play a major role in the etiology of obesity and insulin resistance.;

504 a| Includes bibliographical references (leaves 76-79).;

650 0 a| Metabolismx| Disordersx| Research.=| ^A804;

650 0 a| Mitochondria.=| ^A434;

650 0 a| Peroxisomes.=| ^A389250;

650 0 a| Obesity.=| ^A409;

650 0 a| Insulin resistance.=| ^A251831;

650 0 a| Rats as laboratory animals.=| ^A10876;

650 2 a| Mitochondria.0| (DNLM)D008928=| ^A917755;

650 2 a| Microbodies.0| (DNLM)D008830=| ^A950691;

650 2 a| Obesity.0| (DNLM)D009765=| ^A917747;

650 2 a| Insulin Resistance.0| (DNLM)D007333=| ^A926042;

655 2 a| Academic Dissertation.0| (DNLM)D019478?| UNAUTHORIZED;

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650 7 a| Mitochondria.2| fast0| (OCoLC)fst01024016;

650 7 a| Obesity.2| fast0| (OCoLC)fst01042738;

650 7 a| Peroxisomes.2| fast0| (OCoLC)fst01058335;

650 7 a| Rats as laboratory animals.2| fast0| (OCoLC)fst01090353;

655 7 a| Academic theses.2| fast0| (OCoLC)fst01726453;

655 7 a| Academic theses.2| lcgft;

655 7 a| Thèses et écrits académiques.2| rvmgf0| (CaQQLa)RVMGF-000001173;

700 1 a| Cortright, Robert N.,e| degree supervisor.?| UNAUTHORIZED;

710 2 a| East Carolina University.b| Department of Biology.=| ^A637467;

856 41 z| Access via ScholarShipu| http://hdl.handle.net/10342/12939;

949 a| Click on web addressw| asish| joyner101;

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Peroxisomal enhancement of mitochondrial function / by Tracey L. Woodlief.

Author/creator	Woodlief, Tracey L. author.
Other author	Cortright, Robert N., degree supervisor.
Other author	East Carolina University. Department of Biology.
Format	Theses and dissertations
Production	2005.
Description	99 leaves : illustrations ; 28 cm
Supplemental Content	Access via ScholarShip
Subjects	Metabolism--Disorders. --Research. Mitochondria. Peroxisomes. Obesity. Insulin resistance. Rats as laboratory animals. Mitochondria. Microbodies. Obesity. Insulin Resistance.

Summary	Background: Lipid disposal pathways have been shown to be dysregulated in disease states such as obesity and diabetes, with a main focus of research being on mitochondrial dysfunction. More so, little data exists on peroxisomal function in skeletal muscle, the major tissue responsible for lipid disposal in the healthy or diseased state. Accordingly, it has been hypothesized that mitochondrial impairments in fatty acid oxidation may be compensated for by peroxisomal metabolism of fatty acids to acylcarnintines which can bypass mitochondrial transport mechanisms and enhance efficiency. Purpose: To test the direct effects elevated peroxisomal content on skeletal muscle mitochondrial function. Methods: Peroxisomes and mitochondria I were isolated from rat liver and whole gastrocnemius, respectively, using an Optiprep density gradient system. Oxidation rates (as captured 14CO2 and acid soluble metabolites) were compared via peroxisomal titration experiments under the following conditions: 1) mitochondria plus 1-14C Palmitic Acid (long-chain fatty acid; LCFA) ± malonyl-CoA ± peroxisomes 2) mitochondria plus 1-14C lignoceric acid (very long-chain fatty acid; VLCFA) ± malonyl-CoA ± increasing peroxisomal content. Results: Skeletal muscle mitochondrial oxidation of VLCFA was linearly enhanced in the presence of increasing peroxisomal content. Mitochondrial oxidation of LCFA was not enhanced in the basal state (- malonyl-CoA); however, oxidation of LCFA was increased in the presence of malonyl-CoA, suggesting that peroxisomes represent an alternative pathway for oxidizing LCFA in the disease state characterized by dysfunctional mitochondria. Conclusion: This study is the first to directly demonstrate that increasing peroxisomal content results in increased mitochondrial oxidation of fatty acids, suggesting a viable metabolic target for therapeutic intervention that could lower intramuscular lipids suspected to play a major role in the etiology of obesity and insulin resistance.
General note	Presented to the faculty of the Department of Biology.
General note	Advisor: Ronald N. Cortright
Dissertation note	M.S. East Carolina University 2005
Bibliography note	Includes bibliographical references (leaves 76-79).
Genre/form	Academic theses.
Genre/form	Academic theses.
Genre/form	Thèses et écrits académiques.

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