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049 a| EREE;

050 4 a| QP752.T74b| T56 2002;

100 1 a| Thompson, R. Peter,e| author.;

245 12 a| A morphological quantification of intracellular triglyceride and mitochondria in obese subjects, trained subjects and lean sedentary controls /c| by R. Peter Thompson.;

264 0 c| 2002.;

300 a| vi, 57 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| 2002;

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

500 a| Advisor: Ronald W. Dudek;

520 3 a| In this present study the hypothesis that decreased lipid oxidation within obese individuals can partially be attributed to decreased mitochondria content within skeletal muscle leading to storage of excess lipid as intracellular triglyceride (ICTG) was examined. The results are based on the examination of 11 lean sedentary, 13 obese, and 9 aerobically trained volunteers. Initially, quantitation of Oil Red O staining of muscle biopsies indicated obese subjects with a BMI > 35 kg m-2 had 3.2-fold (P < 0.01) increase in ICTG content when compared to the lean sedentary controls (191.0 ± 33.3 vs. 58.9 ± 6.3 [mu]m2 / 1000 [mu]m2 skeletal muscle). In addition, the trained subjects had a 1.8-fold (P < 0.01) increase in ICTG when compared to the lean sedentary controls (103.4 ± 15.0 vs. 58.9 ± 6.3 [mu]m2 / 1000 [mu]m2 skeletal muscle). The ICTG area of the obese BMI < 35 kg m-2 and lean sedentary controls were very similar, 63.4 ± 20.3 and 58.9 ± 6.3 [mu]m2 / 1000 [mu]m2 skeletal muscle respectively, and no statistical difference was found. There was a strong positive association between levels of ICTG and BMI in both obese populations and the lean sedentary controls (r = 0.77, P < 0.0001). In addition, a strong positive correlation was found between ICTG content and insulin resistance (HOMA value, r = 0.87, P < 0.001). Secondly, mitochondrial area within a portion of the muscle biopsy was determined by digitizing and quantitating transmission electron micrographs. The area of intermyof̕brillar mitochondria in the obese BMI >35 .0 kg m-2 was very similar to the lean sedentary controls (15.0 ± 2.7 [mu]m2 / 1000 [mu]m2 vs. 18.7 ± 2.5 [mu]m2 / 1000 [mu]m2 and no statistical significance was found. However, a negative trend was found between area of ICTG and area of intermyofibrillar mitochondria in obese subjects and lean sedentary controls (r = -0.56, P < 0.1). The area of intermyofibrillar mitochondria in the trained subjects was 2.4-fold higher (P < 0.001) when compared to the lean sedentaiy controls (44.0 ± 3.3 [mu]m2 / 1000 [mu]m2) vs. 18.7 ± 2.5 [mu]m2 / 1000 [mu]m2). In summary, obese subjects BMI > 35 kg m-2 have elevated levels of ICTG, which correlates positively with BMI and insulin resistance. These findings that adiposity is related to both increases in ICTG content and insulin resistance indicates a decrement in lipid oxidation within the obese population. We were unable to demonstrate a significant difference in area of intermyofibrillar mitochondria between the lean sedentary controls and obese subjects suggesting that intermyofibrillar mitochondria are not completely responsible for the reduced lipid oxidation. On the contrary, aerobically trained subjects, with a significant increase in mitochondria and ICTG, to be insulin sensitive. We believe the increased aerobic capacity suggested through increased area of intermyofibrillar mitochondria circumvent any adverse effects of the increased ICTG.;

504 a| Includes bibliographical references (leaves 54-56).;

650 0 a| Triglycerides.;

650 0 a| Lipidsx| Metabolism.;

650 0 a| Mitochondria.;

650 0 a| Muscles.;

650 0 a| Overweight persons.;

650 7 a| Lipidsx| Metabolism.2| fast0| (OCoLC)fst00999374;

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

650 7 a| Muscles.2| fast0| (OCoLC)fst01029953;

650 7 a| Overweight persons.2| fast0| (OCoLC)fst01049461;

650 7 a| Triglycerides.2| fast0| (OCoLC)fst01156700;

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| Dudek, Ronald W.,d| 1950-e| degree supervisor.1| https://id.oclc.org/worldcat/entity/E39PCjJT9C8Vp7hbwfHJgT6Th3;

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

856 41 z| Access via ScholarShipu| http://hdl.handle.net/10342/12714;

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A morphological quantification of intracellular triglyceride and mitochondria in obese subjects, trained subjects and lean sedentary controls / by R. Peter Thompson.

Author/creator	Thompson, R. Peter author.
Other author	Dudek, Ronald W., 1950- degree supervisor.
Other author	East Carolina University. Department of Biology.
Format	Theses and dissertations
Production	2002.
Description	vi, 57 leaves : illustrations ; 28 cm
Supplemental Content	Access via ScholarShip
Subjects	Triglycerides. Lipids--Metabolism. Mitochondria. Muscles. Overweight persons.

Summary	In this present study the hypothesis that decreased lipid oxidation within obese individuals can partially be attributed to decreased mitochondria content within skeletal muscle leading to storage of excess lipid as intracellular triglyceride (ICTG) was examined. The results are based on the examination of 11 lean sedentary, 13 obese, and 9 aerobically trained volunteers. Initially, quantitation of Oil Red O staining of muscle biopsies indicated obese subjects with a BMI > 35 kg m-2 had 3.2-fold (P < 0.01) increase in ICTG content when compared to the lean sedentary controls (191.0 ± 33.3 vs. 58.9 ± 6.3 [mu]m2 / 1000 [mu]m2 skeletal muscle). In addition, the trained subjects had a 1.8-fold (P < 0.01) increase in ICTG when compared to the lean sedentary controls (103.4 ± 15.0 vs. 58.9 ± 6.3 [mu]m2 / 1000 [mu]m2 skeletal muscle). The ICTG area of the obese BMI < 35 kg m-2 and lean sedentary controls were very similar, 63.4 ± 20.3 and 58.9 ± 6.3 [mu]m2 / 1000 [mu]m2 skeletal muscle respectively, and no statistical difference was found. There was a strong positive association between levels of ICTG and BMI in both obese populations and the lean sedentary controls (r = 0.77, P < 0.0001). In addition, a strong positive correlation was found between ICTG content and insulin resistance (HOMA value, r = 0.87, P < 0.001). Secondly, mitochondrial area within a portion of the muscle biopsy was determined by digitizing and quantitating transmission electron micrographs. The area of intermyof̕brillar mitochondria in the obese BMI >35 .0 kg m-2 was very similar to the lean sedentary controls (15.0 ± 2.7 [mu]m2 / 1000 [mu]m2 vs. 18.7 ± 2.5 [mu]m2 / 1000 [mu]m2 and no statistical significance was found. However, a negative trend was found between area of ICTG and area of intermyofibrillar mitochondria in obese subjects and lean sedentary controls (r = -0.56, P < 0.1). The area of intermyofibrillar mitochondria in the trained subjects was 2.4-fold higher (P < 0.001) when compared to the lean sedentaiy controls (44.0 ± 3.3 [mu]m2 / 1000 [mu]m2) vs. 18.7 ± 2.5 [mu]m2 / 1000 [mu]m2). In summary, obese subjects BMI > 35 kg m-2 have elevated levels of ICTG, which correlates positively with BMI and insulin resistance. These findings that adiposity is related to both increases in ICTG content and insulin resistance indicates a decrement in lipid oxidation within the obese population. We were unable to demonstrate a significant difference in area of intermyofibrillar mitochondria between the lean sedentary controls and obese subjects suggesting that intermyofibrillar mitochondria are not completely responsible for the reduced lipid oxidation. On the contrary, aerobically trained subjects, with a significant increase in mitochondria and ICTG, to be insulin sensitive. We believe the increased aerobic capacity suggested through increased area of intermyofibrillar mitochondria circumvent any adverse effects of the increased ICTG.
General note	Presented to the faculty of the Department of Biology.
General note	Advisor: Ronald W. Dudek
Dissertation note	M.S. East Carolina University 2002
Bibliography note	Includes bibliographical references (leaves 54-56).
Genre/form	Academic theses.
Genre/form	Academic theses.
Genre/form	Thèses et écrits académiques.

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