UVM Theses and Dissertations
Format:
Print
Author:
Rice, Beth H.
Dept./Program:
Animal, Nutrition and Food Sciences Program
Year:
2011
Degree:
Ph. D.
Abstract:
Dietary trans-fatty acids (tFA) are derived primarily from two sources; industrially-produced (IP)-tFA are present in partially hydrogenated vegetable oils (PHVO) and ruminant produced (RP)-tFA are naturally occurring in the milk and meat of ruminant animals. Consumption of IP-tFA has been positively associated with risk of coronary heart disease (CHD), innate immune dysfunction, and other abnormal metabolic conditions. RP-tFA intake has been inversely associated with CHD risk, particularly in women. Ruminant products typically contain less than 10% of total fat as tFA, with the predominant isomer being trans-11 18:1. In contrast, PHVO often contain up to 60% of total fat as tFA, with the predominant isomers being trans-6-8; trans-9, and trans-10 18:1. The differences in both the relative amount as well as the distribution of tFA in ruminant and industrial sources may be responsible for their divergent effects on metabolic health.
It was hypothesized that when consumed at the same level, tFA from ruminant and industrial sources would be metabolized differently; consumption of RPtFA would be inversely associated with CHD and consumption of IP-tFA would lead to the development of atherosclerotic lesions. The objective was to directly compare diets rich in RP-tFA and IP-tFA from butter oil (BO) and PHVO, respectively. Whereas the BO diet was rich in trans-ll 18:1 and low in trans-6-8, trans-9, and trans-10 18:1, the PHVO diet was high in trans-6-8, trans-9, and trans-10 18:1 fatty acids and low in trans 11 18:1. The total tFA content was equal between the BO and PHVO treatments, making the trans-18: 1 distribution the difference between the two.
Hartley guinea pigs were the chosen model because they metabolize fatty acids similarly, to humans, and have been shown previously as suitable for studying the effects of dietary lipids on metabolic disorders. When fed at the same high dose, RP-and IP-tFA did not differ in their effect on plasma lipids or lipoproteins in male or female guinea pigs. Plasma and hepatic lipids did not differ in response to treatments in females with intact ovaries (OV) or those that had been ovariectomized (OVX) to mimic the postmenopausal condition. Neither dietary source of tFA induced atherosclerotic lesions in male guinea pigs, a parameter that was not tested in females. RP-tFA raised plasma total and small high-density lipoprotein (HDL) particle subclass concentrations and decreased mean HDL particle size in male and female guinea pigs.
Large HDL particle subclass concentrations were higher in OV than OVX females fed BO. In both male and female guinea pigs, RP-and IP-tFA were incorporated into tissues within eight weeks of consuming the experimental treatments, and were indicative of the diets consumed. The accumulation of tFA in tissues differed between diets within tissues; while within diets, it varied across tissues. Results indicated that the consumption of equally high amounts of RP-and IP-tFA did not lead to the development of CHD in male Hartley guinea pigs. RP-tFA consumption may have led to a desirable plasma lipoprotein profile, which could not be confirmed because none of the guinea pigs developed atherosclerotic lesions. The varying incorporation of RP-and IP-tFA in and across tissues warrants further investigation. In conclusion, when fed at the same level, IP-and RP-tFA from BO and PHVO were differentially metabolized in both males and females, but neither led to the development of CHD.
It was hypothesized that when consumed at the same level, tFA from ruminant and industrial sources would be metabolized differently; consumption of RPtFA would be inversely associated with CHD and consumption of IP-tFA would lead to the development of atherosclerotic lesions. The objective was to directly compare diets rich in RP-tFA and IP-tFA from butter oil (BO) and PHVO, respectively. Whereas the BO diet was rich in trans-ll 18:1 and low in trans-6-8, trans-9, and trans-10 18:1, the PHVO diet was high in trans-6-8, trans-9, and trans-10 18:1 fatty acids and low in trans 11 18:1. The total tFA content was equal between the BO and PHVO treatments, making the trans-18: 1 distribution the difference between the two.
Hartley guinea pigs were the chosen model because they metabolize fatty acids similarly, to humans, and have been shown previously as suitable for studying the effects of dietary lipids on metabolic disorders. When fed at the same high dose, RP-and IP-tFA did not differ in their effect on plasma lipids or lipoproteins in male or female guinea pigs. Plasma and hepatic lipids did not differ in response to treatments in females with intact ovaries (OV) or those that had been ovariectomized (OVX) to mimic the postmenopausal condition. Neither dietary source of tFA induced atherosclerotic lesions in male guinea pigs, a parameter that was not tested in females. RP-tFA raised plasma total and small high-density lipoprotein (HDL) particle subclass concentrations and decreased mean HDL particle size in male and female guinea pigs.
Large HDL particle subclass concentrations were higher in OV than OVX females fed BO. In both male and female guinea pigs, RP-and IP-tFA were incorporated into tissues within eight weeks of consuming the experimental treatments, and were indicative of the diets consumed. The accumulation of tFA in tissues differed between diets within tissues; while within diets, it varied across tissues. Results indicated that the consumption of equally high amounts of RP-and IP-tFA did not lead to the development of CHD in male Hartley guinea pigs. RP-tFA consumption may have led to a desirable plasma lipoprotein profile, which could not be confirmed because none of the guinea pigs developed atherosclerotic lesions. The varying incorporation of RP-and IP-tFA in and across tissues warrants further investigation. In conclusion, when fed at the same level, IP-and RP-tFA from BO and PHVO were differentially metabolized in both males and females, but neither led to the development of CHD.