Access Type

Open Access Dissertation

Date of Award

January 2011

Degree Type


Degree Name



Nutrition and Food Science

First Advisor

Pramod Khosla


Consumption of trans-fatty acids (tFA) and saturated fatty acids (SFA) have been associated with higher incidence of coronary heart disease. Experimental and observational data suggests that consumption of PHVO containing tFA, like SFA leads to increased total cholesterol and LDL-cholesterol (LDL-C) but compared to tFA, SFA raises HDL-cholesterol (HDL-C). An attempt to eliminate PHVO from the food supply has resulted in the need to find alternatives which despite their higher dietary fat saturation as compared to naturally occurring vegetable oils, may be preferable to PHVO. However, amongst SFA, the effects on plasma lipoproteins are variable. Thus, we hypothesized that specific combinations of dietary SFA will not contribute to an adverse lipid profile.

We used gerbils and hamsters as our study models to determine the effects of Lauric and Myristic Acid (Hi-LM), Oleic Acid (Hi-OL), Palmitic Acid (Hi-PO), Linoleic Acid (Hi-LO Low-LN), Stearic acid and Linoleic Acid (Hi-SLO) supplemented diets on plasma and liver lipids and lipoproteins. The results revealed that compared to the Hi-LM diet, all diets had lower TC, LDL-C and HDL-C. Liver lipids were similar for all the diet groups. Also, we analyzed the gene expression for the reverse Cholesterol transport genes. No significant differences in ABCA1, ApoA1, CETP or SR-B1 were observed between the diet groups compared with Hi-LM diet. The data suggested no additional adverse effects on CHD risk factors compared with Hi-LM diet.

Carbohydrates are generally considered a safe replacement for SFA. We used a hamster model to evaluate the extent to which the amount and type of SFA affect lipoproteins. Diets were formulated such that percentage of calories from protein, MUFA and PUFA were kept constant while calories from Lauric and Myristic (60%LM, 45%LM, 30% LM) or Palmitic Acid (45%PA, 30% PA) were replaced with calories from carbohydrate and compared to 21% CON diet. Plasma TC and n-HDL-C was lower in all diet groups compared with 60%LM and 45% LM supplemented groups. Liver lipids were similar in all diet groups. Analysis of Reverse Cholesterol Transport genes revealed no significant differences in expression between the diet groups compared with 21% CON. Data suggests no adverse effect of PA at any level of consumption and no net effect of replacing CHO for at any level of SFA.

The postprandial state is a reflection of the metabolic state in humans due to regular diet intake. We used an oral challenge to test oils with various fatty acid compositions (Hi-PO, Hi-LO and Hi-OL) to evaluate postprandial changes in lipids at 0, 2, 4 and 8 hours. No significant differences were seen in TC, HDL-C, TC:HDL-C and TG between the test oils. We analyzed the chylomicron fractions following the oral fat challenge and data revealed no significant differences in the chylomicron fractions between the test oils. Additionally, we measured CETP activity in plasma following the challenge and no significant differences were observed. The data suggests in agreement with the hypothesis, oil formulations with specific SFA will not cause any adverse effects in lipids and lipoproteins.