Triglyceride composition of naked-seed pumpkin seed oil

The triglyceride (TG) structure of naked-seeded pumpkin seed oil (Cucurbita pepo, var. Lady Godiva) was determined. Crude oil of naked-seeded pumpkin seed was extracted from dried, ground whole seeds, alkali refined, bleached and deodorized. The oil was separated into four fractions by low temperature crystallization at 10 degree intervals from -30 to 0°C. The refined oil and oil in each fraction were hydrolyzed by pancreatic lipase, and the 2-monoglyceride was isolated by thin layer chromatography. Fatty acid composition of the refined oil, the oil in each fraction and the respective 2-monoglyceride were determined by gas chromatography. The fatty acid composition in the refined oil was 14.96% palmitic, 4.78% stearic, 49.11% oleic, 30.87% linoleic and 0.28% linolenic. Percentages of alignment structure of the triglycerides molecules (ASTM) of the oil from the naked-seeded pumpkin seed were calculated to be; SSS = 0.28, SSU = 1.63, SUS = 6.42, USU = 2.32, SUU = 36.75 and UUU = 52.88; where S = saturated fatty acid and U = unsaturated fatty acid. The main glycerides of the oil where S = saturated, 0 = oleic and U = linoleic plus linolenic were found to be SOO = 13.82%, OOU = 13.32%, 000 = 12.38%, OUU = 10.59% and OUS = 10.99%. The oil on fractionation by low temperature crystallization yielded two major fractions, C fraction at -10°C representing 27.95% of total oil, and D fraction, liquid at 0°C representing 44.4% of the total oil. In ASTM, fraction C had larger amounts of UUU, USU and SSU, and fraction D had larger amounts of SUU, SUS and SSS. The triglyceride composition was confirmed by quantitative fractional crystallization of the refined oil and by triglyceride determination in each fraction and calculation of the original triglycerides from the triglycerides of each fraction

Effects of Carnitine on Ethanol-Induced Hepatic Steatosis

The lipotropic and hypolipidemic effects of carnitine and its precursors, namely lysine (Lys) and methionine (Met), was examined in male Sprague-Dawley rats fed ethanol as 36% of the total calories for a duration of 56 days (Experiment I). Ethanol produced significant hepatic steatosis and hypertriglyceridemia as evidenced from elevated concentrations of total lipids, triglycerides, cholesterols, and phospholipids. Supplementation of the ethanol diet with 1.0% D,L-carnitine and 0.5% L-Lys plus 0.2% L-Met significantly reduced ethanol-induced elevation of the various lipid classes with the exception of free fatty acids. The triglyceride contents in liver and plasma were inversely related to the concentrations of carnitine, acylcarnitines, and total carnitine. The effects of a combination of carnitine and its precursors were not greater than those of carnitine alone. It is suggested, therefore, that a deficiency of functional carnitine may exist in a chronic alcoholic state which can be improved by dietary carnitine. In two following experiments, animals were fed the ethanol liquid diets supplemented with various levels (Experiment II: 0.0, 0.2, 0.6, 1.0, and 2.0%; Experiment III: 0.0, 0.1, 0.5, 0.8, 1.2, and 1.6%) of D,L-carnitine for 28 and 45 days. In the 28 day experiment, the effects of supplemental carnitine were significant only in the plasma triglycerides and reduction in hepatic lipid classes were minimal. In the 45 day experiment, various lipid classes of the alcohol-compromised liver and plasma were significantly reduced with carnitine treatment, and the effect was dose-dependent. The optimum lipotropic and hypolipidemic effect were produced by 0.8% D,L-carnitine. thus it is concluded that in rats, supplemental D,L-carnitine ameliorated ethanol-induced hyperlipidemia and hepatic steatosis in a dose-dependent manner