The effect of source of dietary carboyhydrate upon the concentration and distribution of phospholipids in the fractions of human blood was studied. Three healthy women received diets which contained 16% of the calories as protein, 40% as fat, and 44% as carbohydrate. During the four dietary periods of six days each, 80% of the carbohydrate was supplied alternately by sucrose (Sugar Diet) or by polysaccharides from natural sources (Complex Diet). Blood samples were drawn before breakfast on the final day of each dietary period. The total lipid, lipid phosphorus, and distribution of phospholipids were determined in erythrocytes, leukocytes, platelets, and plasma. Clotting time of the platelet-rich plasma of the subjects was determined. In periods of this length, no consistent changes in the blood lipids could be detected. The Sugar Diet appeared to increase the proportion of phosphatidyl choline and decrease the proportion of sphingomyelin slightly in the plasma and platelets. The phosphatidyl choline fraction of the leukocyte phospholipids decreased slightly after the Sugar Diet. No relationship was observed between in vitro coagulation time and the distribution of phospholipids in the blood fractions. One subject did demonstrate a marked increase in coagulation time after the diet containing complex carbohydrate. / Graduation date: 1969

The interrelationships between physical measurements, dietary intake of specific nutrients, and plasma lipids were examined in 19 healthy elderly subjects. The mean blood pressures, relative weights, and skinfold thicknesses were within normal ranges, although women tended to be more overweight. Systolic pressure and relative weight were associated with increased body fatness, as measured by suprailiac and subscapular skinfolds. On the average, the caloric intake of these subjects was only 85% of the recommended dietary allowance; carbohydrate supplied 48% and fat accounted for 33% of the calories. The subjects consumed a low level of saturated fatty acids and cholesterol but the dietary ratio of polyunsaturates to saturates was similar to that of the typical American diet. Higher levels of dietary fat were associated with higher intakes of saturated fatty acids and cholesterol. The mean concentrations of cholesterol, phospholipids, and triglycerides in plasma were within the normal reported ranges; these lipid fractions appeared to be uninfluenced by the composition of the diet. The concentration of nonesterified fatty acids in plasma was unusually high and positively correlated with age of the subjects. There was also an unexplained correlation between plasma nonesterified fatty acids and the linoleic acid content of the diet. / Graduation date: 1976

Malonaldehyde, a three carbon dialdehyde, is one of the numerous carbonyl compounds associated with oxidative deterioration of food lipids. It is assumed to be formed as a product of lipid autoxidation occurring according to the generally accepted free radical mechanism. This compound is of great interest because of its potential high reactivity and its wide occurrence in autoxidized lipids. Malonaldehyde may participate in eliciting some of the adverse biological and chemical effects of in vitro and in vivo lipid autoxidation. In this investigation a micro 2-thiobarbituric acid analysis for malonaldehyde in various biological materials was developed; the acute toxicity, subacute toxicity and associated physiological responses were determined; and the reaction of malonaldehyde with glycine and protein was investigated. The single oral median lethal dose (LD₅₀) of malonaldehyde administered to rats as the ethoxy derivative, 1, 1, 3, 3-tetraethoxy propane, and the enolic sodium salt, sodium beta-oxyacrolein, was found to be 527 mg (slope function 1.67) and 632 mg (slope function 1.23) per kg body weight respectively. The LD₅₀ of malonaldehyde determined with sodium beta-oxyacrolein was the more accurate estimation of its acute toxicity. Subacute feeding of rats malonaldehyde as the ethoxy derivative, 1, 1, 3, 3-tetraethoxypropane, and as the sodium salt of the enamine derivative of glycine, sodium N-prop-2-enal amino acetate, elicited a series of similar varied and marked anatomical, physiological and/ or biochemical changes over control animals. Ingested malonaldehyde was largely metabolized or altered so that it was no longer detectable by reaction with 2-thiobarbituric acid. It was distributed throughout the body and particularly in the blood and glandular tissue. Dietary malonaldehyde was found to be concentrated in erythrocytes where it had apparently reacted in vivo with the intracellular protein, tentatively with hemoglobin. A decreased growth rate, a lowered diet utilization, varying degrees of anemia, increased organ weights, symptoms of various vitamin deficiencies, and abnormal nitrogen and tryptophan metabolism were observed. Histomorphological damage to liver tissue included a lytic necrosis of parenchymal cells, increased parenchymal cell and nuclear size, bile ductular proliferation with vacuolation of parenchymal cytoplasm with cyst formation. The response to dietary malonaldehyde probably involved both a dirept toxic action at the cellular level and an interaction with some fraction(s) of the diet altering its nutrient value. The reaction of malonaldehyde with glycine was found to yield the enamine, N-prop-2-enal amino acetic acid. The reaction was shown to conform to a S [subscript n] 2 mechanism. The rate of the reaction was shown to be highly dependent on the hydrogen ion concentration. The maximum observed reaction rate was found near pH 4.20. A postulated mechanism for the reaction involves the nucleophilic 1, 4-addition of the amino nitrogen of glycine to the end carbon atom of the alpha, beta-unsaturated carbonyl system of the enol of malonaldehyde. The reaction of malonaldehyde with bovine plasma albumin was shown to involve the e-amino lysine and N-terminal amino aspartic acid functions as judged by their loss to reaction with 1-fluoro-2, 4- dinitrobenzene. The rate of the reaction was dependent on the hydrogen ion concentration with a maximum observed reaction rate near pH 4.30. Malonaldehyde did not appear to participate in an intermolecular cross-linking reaction as judged by the lack of viscometric hardening of gelatin sols. Presumptive evidence for the reaction of malonaldehyde, derived from autoxidized lipids, and the ε-amino lysine functions of bovine plasma albumin was obtained. A postulated mechanism for the reaction of malonaldehyde with protein involves the nucleophilic 1,4-addition of the free amino functions on the protein to the end carbon atom of the alpha, beta-unsaturated carbonyl system of the free enol to form an enamine linkage. / Graduation date: 1966

Diets containing cyclopropenoid fatty acids (CPFA) were fed to rainbow trout. At a level of 223 ppm (from Sterculia foetida oil), these CPFA in six weeks reduced weight gain by as much as 50 percent over the control fish on the same diet without CPFA. Compounds containing the intact cyclopropene ring were recovered from the tissue lipids of the trout at approximately two-thirds of the level fed. These acids seemed to concentrate in the egg lipids of the adult female fish. At 223 and 2233 ppm (from S. foetida oil) and 50 ppm (from food grade cottonseed flour) the CPFA were demonstrated to alter lipid metabolism. In general, the CPFA fed fish had higher stearic and palmitic acid levels and lower oleic and palmitoleic acid levels in their tissue lipids than did the controls. On diets containing corn oil or corn oil plus salmon oil, fish fed CPFA tended to deposit more long chain unsaturated fatty acids than did their controls. When provided with tristearin as the sole dietary lipid, the CPFA fed fish reduced the level of unsaturation of their tissue lipids. / Graduation date: 1967

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Primary cultures of human umbilical vein endothelial cells were incubated with n-3 and n-6 fatty acids for a maximum of 24 hours, to investigate their distribution in membrane neutral lipids and phospholipid. Furthermore, the release of labelled free fatty acids due to induction of PLA2 by cytokines and the further production of PGI2 in cells supplemented with different PUFA was investigated in the present study to elucidate the metabolism of lipids in these cells. In addition, the extent of lipid peroxidation and the potency of antioxidants in inhibiting the formation of lipid peroxides due to dietary modification in cells were also investigated in relation to their effects on essential fatty acid metabolism. Endothelial cells in the present study had a significant capacity to metabolise PUFA which was supplied exogenously. PUFA of n-3 and n-6 families behaved differently with respect to their incorporation into membrane lipids. ARA of n-6 family had the greatest incorporation into the total lipids compared to n-3 PUFA ie, EPA and DHA. About 80% of PUFA was incorporated into the phospholipid fraction and another 20% was found in neural lipids. [14C]-ARA and [14C]-DHA when co-incubated with endothelial cells for longer incubation periods were found mainly incorporated into TAG. In contrast, [14C]-EPA was distributed significantly into other fractions of neutral lipids with no significant increase in the TAG fraction. TAG is important as a fatty acid store in the cells including essential PUFA which can be metabolised and utilised for PG synthesis during the deficiency of eicosanoid precursor (PUFA) in the phospholipids of cell membranes. All the PUFA tested were incorporated into PC to a similar extent with time. Transfer between PC and PE during the longer incubation time was observed in the present study which indicated that PE may be important in the storage of fatty acids in phospholipids since PC and PI were the most preferred substrates for the phospholipases.

No description available.

While adhering to an active lifestyle has been associated with a more favorable lipid profile and reduced risk of coronary heart disease (CHD), information regarding the optimal training modality is not well defined. This project examined the acute and chronic effects of endurance (ET), resistance (RT), and combination endurance / resistance (CT) exercise on lipid metabolism and non-traditional CHD risk markers in untrained men. Thirty-one subjects were randomly assigned to participate for 12 weeks in one of three exercise groups: ET, RT, or CT. To measure the effects of acute exercise on lipid metabolism, fasting blood samples were obtained before (baseline) and 24 hours after (24 h) acute exercise (treadmill jogging at 70% V . O2peak, 350 kcals; weight lifting exercise at 70% of 1RM; combination of treadmill jogging and weight lifting at 70% maximal capacity, 350 kcals). Blood variables were adjusted for plasma volume shifts. This acute exercise protocol was completed on two different occasions corresponding to 0 and 12 weeks of training. For acute exercise (pre-training), significant results of a 3 (Group) x 2 (Time) ANOVA, repeated for Time, (p < 0.05) were as follows: TC, HDL-C, HDL2&3-C were lower 24 h after exercise in the RT group. HDL2-C was higher 24 h after exercise in the CT and ET groups. In the ET group, LDL1-C was elevated 24 h after exercise. With all groups combined, LDL3-C and the TC / HDL-C ratio were elevated and LDL2-C decreased 24 h after exercise. For exercise training, significant results of a 3 (Group) x 2 (Training Period) ANOVA, repeated for Training Period, (p < 0.05) were as follows: Body Fat, LDL2-C, and apo A-I were lower after training. Changes in other lipid variables were similar in untrained males performing different types of exercise training. For acute exercise (post-training), significant results of a 3 (Group) x 2 (Time) ANOVA, repeated for Time, (p < 0.05) were as follows: TC, HDL-C, HDL2-C, LDL-C, NONHDL-C, VLDL-C, IDL-C, LDL3-C, LDL density, and LPLa were all higher 24 h after exercise. Post-exercise changes in the dependent variables were similar in trained males performing different types of exercise.