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Alterations in growth, lipid metabolism and P:O ratios in mice fed Sterculia foetida oilLehman, Michael Wesley 28 June 1974 (has links)
Cyclopropenoid fatty acids (CPFA) are natural components of
cottonseed oil, a major food oil in the United States. The ability of
CPFA to cause abnormal biochemical and physiological effects when
fed to laboratory and farm animals has prompted an investigation of
their effects on mice.
Between 0.05 and 0.55% CPFA were fed as glycerines of
Sterculia foetida oil (SFO, containing 55% CPFA) to mice to determine
their effect on certain aspects of growth, lipid metabolism and
mitochondrial function.
One-half percent SFO fed to weanling mice caused a small
temporary decrease in growth rate when compared to controls. Many
mice fed 1% SFO stopped growing and died by the end of a 9-week
feeding trial. Mice fed less than 1% SFO, or 1% SFO for shorter
periods of time, showed increased liver-to-body-weight ratios, accumulation of CPFA in adipose tissue and increased ratios of
16:0/16:1, 18:0/18:1 and total saturated to unsaturated fatty acids in
liver and depot fat. Erythrocytes from CPFA-fed mice hemolyzed
more slowly than erythrocytes from control mice in isotonicnonelectrolytes,
implying an effect of CPFA on membrane lipid composition.
One-half percent SFO fed for 9 to 31 days inhibited almost
completely the incorporation of [¹⁴c] from labeled palmitate or
acetate into liver monounsaturated fatty acids. At the same time,
0.5% SFO retarded the incorporation of label from acetate into
¹⁴C₂ and total liver lipid, but stimulated twofold the incorporation
into liver sterols. The oxidation of labeled palmitate was also
reduced. CPFA caused lipid accumulation in livers.
P:0 ratios of liver mitochondria from mice fed 1% SFO for 6 to
15 days were 1.06- 1.45 while control P:0 ratios were 2.30-2.85.
The decrease was due to decreased phosphorylation, but increased
respiration. The relationship between the observed results and
membrane fatty acid composition was discussed. / Graduation date: 1975
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Respiration of cyclopropenoid fatty acids in vitroLiu, Rosa L. C. Hsu, 1939- January 1970 (has links)
No description available.
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Comparative effects of sterculic and malvalic acids on the hepatic microsomal cytochrome P-450 system of rainbow trout (Salmo gairdneri)Bailey, Marcia Lynn 04 December 1978 (has links)
Graduation date: 1979
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Metabolism of (1-¹⁴C) linolenic acid in coho salmon, Oncorhynchus kisutchParker, Robert S. 05 May 1978 (has links)
Graduation date: 1978
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Bijdrage tot de physiologie van de essentiele vetzurenDam, Frans Jacob van. January 1900 (has links)
Academisch Proefschrift--Amsterdam. / English summary: p. 76-77. "Literatuur" p. 79-83.
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The essential fatty acid requirements of rainbow trout (Salmon gairdneri)Castell, John Daniel 02 February 1970 (has links)
Graduation date: 1970
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SERUM FREE FATTY ACID CONCENTRATION DURING POST-EXERCISE RECOVERY (INSULIN, HUNGER).MAXWELL, BESS DEVERE. January 1985 (has links)
In order to achieve a better understanding of the impact of exercise on the concentration of serum free fatty acids (FFA) during post-exercise recovery, the purposes of this study were: (1) to determine the relationships between exercise intensity, total exercise energy expenditure, and the concentration of serum FFA during post-exercise recovery; (2) to examine the effects of exoge- nous glucose on post-exercise serum FFA and hormones controlling the FFA response; and (3) to examine the impact of acute exercise on hunger. Untrained, 12-h fasted, college-age males performed cycle ergometer exercise at exercise intensities ranging from 29 to 59% peak ‘VO₂ for total energy expenditures ranging from 162 to 320 kcal. Blood samples, hunger ratings, and metabolic indices were collected or measured before, during, and for 3 h post-exercise. In response to exercise of approximately 300 kcal, FFA was elevated for 3 h post-exercise. The FFA response was a function of total exercise energy expenditure, rather than exercise intensity, or combined effects of these factors. The response was associated with low insulin concentration but no changes were observed in blood glucose, glucagon, growth hormone, or cortisol. Glucose ingestion and infusion studies demonstrated that possible mechanisms con- tributing to the post-exercise FFA response included decreases in FFA re-esterification, increases in triglyceride hydrolysis, and decreases in sympathetic input to adipose tissue. Exercise caused a suppression of hunger for 2 h post-exercise which was a function of the combined effects of exercise intensity and total energy expenditure. An increase in core temperature may have contributed to the anorexigenic effect of exercise. In conclusion, exercise, performed in and followed by a period of fasting caused an elevation of FFA for 3 h during post-exercise recovery. The post-exercise recovery period should be considered an important phase in the physiological impact of exercise on the storage and utilization of fat.
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Maternal docosahexaenoic acid (DHA) supplementation and fetal DHA accretionMontgomery, Colette January 2001 (has links)
No description available.
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Weight cycling--: induced alteration in fatty acid metabolism.January 1998 (has links)
by Sea Man Mei, Mandy. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 203-214). / Abstract also in Chinese. / ACKNOWLEDGMENTS --- p.i / ABSTRACT --- p.ii / LIST OF ABBREVAIATIONS --- p.vi / TABLE OF CONTENTS --- p.vii / Chapter Chapter1 --- General Introduction / Chapter 1.1 --- DEFINITION --- p.2 / Chapter 1.2 --- MOTIVATION OF THE ONSET OF WEIGHT CYCLING --- p.3 / Chapter 1.3 --- PHYSIOLOGICAL EFFECTS OF WEIGHT CYCLING --- p.6 / Chapter 1.3.1 --- """Dieting-Induced Obesity"" Hypothesis" --- p.6 / Chapter 1.3.1.1 --- Food Efficiency --- p.6 / Chapter 1.3.1.2 --- Proposed Mechanisms for the Increase of Food Efficiency --- p.10 / Chapter 1.3.1.3 --- Change in Body Fat --- p.14 / Chapter 1.3.2 --- Association with Increased Mortality and Coronary Heart Disease (CHD) --- p.15 / Chapter Chapter2 --- Depletion of Linoleic Acid and α-Linolenic Acid Caused by Weight Cycling is Independent of the Extent of Calorie-Restriction / Chapter 2.1 --- INTRODUCTION --- p.18 / Chapter 2.1.1 --- Nomenclature of Fatty Acids --- p.18 / Chapter 2.1.2 --- Metabolism and Physiological Roles of LA and α-LnA --- p.19 / Chapter 2.1.2.1 --- "LA, α-LnA and their Derivatives as Structural Components" --- p.21 / Chapter 2.1.2.2 --- Production of Eicosanoids from LA and α-LnA --- p.22 / Chapter 2.1.2.3 --- Other Physiological Roles --- p.23 / Chapter 2.1.3 --- Dietary LA and α-LnA Relative to CHD --- p.24 / Chapter 2.1.3.1 --- Dietary LA and CHD --- p.24 / Chapter 2.1.3.2 --- Dietary α-LnA and CHD --- p.26 / Chapter 2.1.4 --- WC-Induced Alteration in the Composition of Tissue Lipids --- p.27 / Chapter 2.2 --- OBJECTIVE OF THE PRESENT STUDY --- p.29 / Chapter 2.3 --- MATERIALS AND METHODS --- p.30 / Chapter 2.3.1 --- Animals and Diets --- p.30 / Chapter 2.3.2 --- Lipid Analysis --- p.32 / Chapter 2.3.3 --- Triacylglycerol Species Analysis --- p.34 / Chapter 2.3.4 --- Other Assays --- p.35 / Chapter 2.3.5 --- Statistics --- p.35 / Chapter 2.4 --- RESULTS --- p.36 / Chapter 2.4.1 --- Food Intake --- p.36 / Chapter 2.4.2 --- Change of Body weight --- p.38 / Chapter 2.4.3 --- Weight of Liver and Adipose Tissues --- p.40 / Chapter 2.4.4 --- Serum Cholesterol and Triglycerides --- p.41 / Chapter 2.4.5 --- Carcass Total Fatty Acids --- p.42 / Chapter 2.4.6 --- Adipose Tissue Fatty Acids --- p.44 / Chapter 2.4.7 --- Liver Fatty Acids --- p.47 / Chapter 2.5 --- DISSCUSION --- p.50 / Chapter Chapter3 --- Influence of Dietary Fat Level on Fatty Acid Composition and Adiposity in Weight-Cycled Rats / Chapter 3.1 --- INTRODUCTION --- p.56 / Chapter 3.1.1 --- Fat Preference and Intake in Humans --- p.56 / Chapter 3.1.2 --- Alteration of Lipid Metabolism Induced by Dietary Fat --- p.58 / Chapter 3.1.3 --- Interaction Between Weight Cycling and Fat Intake --- p.60 / Chapter 3.2 --- OBJECTIVE OF THE PRESENT STUDY --- p.62 / Chapter 3.3 --- MATERIALS AND METHODS --- p.63 / Chapter 3.3.1 --- Animals and Diets --- p.63 / Chapter 3.3.2 --- Analysis of Adipocytes --- p.66 / Chapter 3.3.3 --- Fatty Acid Analysis --- p.67 / Chapter 3.3.4 --- "Determination of Serum Cholesterol, Triglycerides and Glucose" --- p.68 / Chapter 3.3.5 --- Statistics --- p.68 / Chapter 3.4 --- RESULTS --- p.69 / Chapter 3.4.1 --- Body Weight --- p.69 / Chapter 3.4.2 --- Food Intake and Food Efficiency --- p.71 / Chapter 3.4.3 --- Weight of Liver --- p.74 / Chapter 3.4.4 --- Weight of Adipose Tissue --- p.74 / Chapter 3.4.5 --- Number and Size of Adipocytes --- p.81 / Chapter 3.4.6 --- "Serum Triglycerides, Cholesterol and Glucose" --- p.85 / Chapter 3.4.7 --- Fatty Acid Composition --- p.92 / Chapter 3.5 --- DISCUSSION --- p.145 / Chapter 3.5.1 --- Weight Cycling-Induced Obesity Only with a High-Fat Diet --- p.145 / Chapter 3.5.1.2 --- Effect of Weight Cycling on the Size of Adipocytes --- p.147 / Chapter 3.5.1.3 --- Food Efficiency during Weight Cycling --- p.148 / Chapter 3.5.2 --- Weight-Cycling Induced Specific Alteration of Fatty Acid Metabolism --- p.149 / Chapter Chapter4 --- Weight Cycling Altered the Activities of Lipoprotein Lipase and Lipogenic Enzymes in Rats / Chapter 4.1 --- INTRODUCTION --- p.152 / Chapter 4.1.1 --- Fatty Acid Metabolism --- p.152 / Chapter 4.1.1.1 --- Fatty Acid Synthesis --- p.152 / Chapter 4.1.1.2 --- Fatty Acid Storage --- p.155 / Chapter 4.1.1.3 --- Fatty Acid Oxidation --- p.156 / Chapter 4.1.2 --- Hormonal Control of Fatty Acid Metabolism During Fasting and Refeeding --- p.158 / Chapter 4.1.2.1 --- Fatty Acid Metabolism During Fasting --- p.158 / Chapter 4.1.2.2 --- Fatty Acid Metabolism During Fed-State --- p.160 / Chapter 4.2 --- OBJECTIVE OF THE PRESENT STUDY --- p.161 / Chapter 4.3 --- MATERIALS AND METHODS --- p.162 / Chapter 4.3.1 --- Samples --- p.162 / Chapter 4.3.2 --- Enzymatic Analysis --- p.162 / Chapter 4.3.2.1 --- Lipoprotein Lipase (LPL; EC 3.1.1.34) --- p.162 / Chapter 4.3.2.2 --- Fatty Acid Synthase (FAS; EC 2.3.1.85) --- p.165 / Chapter 4.3.2.3 --- Malic Enzyme (ME; EC 1.1.1.40) --- p.166 / Chapter 4.3.2.4 --- Pyruvate Kinase (PK; EC 2.7.1.40) --- p.166 / Chapter 4.3.2.5 --- Acetyl-CoA Carboxylase (ACC; EC 6.4.1.2) --- p.167 / Chapter 4.3.2.6 --- "Phosphoenolpyruvate Carboxykinase (PEPCK, EC 4.1.1.32)" --- p.168 / Chapter 4.3.2.7 --- Determination of Protein Content --- p.169 / Chapter 4.3.3 --- Determination of Serum Insulin and Serum Glucagon --- p.169 / Chapter 4.3.4 --- Statistics --- p.169 / Chapter 4.4 --- RESULTS --- p.170 / Chapter 4.4.1 --- Enzymatic Analysis --- p.170 / Chapter 4.4.1.1 --- Lipoprotein Lipase --- p.170 / Chapter 4.4.1.2 --- Fatty Acid Synthase --- p.175 / Chapter 4.4.1.3 --- Malic Enzyme --- p.182 / Chapter 4.4.1.4 --- Pyruvate Kinase --- p.182 / Chapter 4.4.1.5 --- Acetyl-CoA Carboxylase --- p.187 / Chapter 4.4.1.6 --- Phosphoenolpyruvate Carboxykinase --- p.187 / Chapter 4.4.2 --- Level of Serum Insulin and Glucagon --- p.192 / Chapter 4.5 --- DISCUSSION --- p.196 / Chapter 4.5.1 --- Effect of Weight Cycling on Activity of Lipoprotein Lipase and Lipogenic Enzymes Activity --- p.196 / Chapter 4.5.2 --- The Overshoot of Enzymatic Activities in Relation to Tissue Fatty Acid Composition --- p.198 / Chapter 4.5.3 --- No Elevation of Plasma Insulin in Weight Cycled Rats --- p.199 / Chapter Chapter5 --- Conclusion --- p.200 / References --- p.203
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Dietary fatty acids and the metabolic response to realimentation following starvation in rats.Arès, Marie Denise. January 1969 (has links)
No description available.
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