Differential Effects of Dietary Methyl Esters of Long-Chain Saturated and Polyunsaturated Fatty Acids on Rat Liver and Adipose Tissue Lipogenesis

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Abstract
Four experiments were conducted to investigate what influence methyl esters of C16:0, C18:0, C18:1, C18:2, and C18:3 fatty acids exert on rat liver and adipose tissue fatty acid synthesis and related enzymes when supplemented to a fat-free diet (FF). A randomized complete block design, in which rats were matched for body weight and food intake, was utilized. Rats previously adapted to a meal-eating regimen (access to food from 0900 to 1200 hours) were fed a FF-diet for 7 days prior to the addition of the respective dietary fatty acids. In experiments 1 to 3, all esters were supplemented at a level of 3% of the daily FF-diet allotment. The apparent absorbabilities of C16:0 and C18:0 were determined to be 40% and 35%, while values for C18:1, C18:2, and C18:3 were 88%, 87%, and 89%, respectively. In comparison to the FF dietary treatment, polyunsaturated fatty acids (C18:2 and C18:3) were able in three of four experiments to reduce the rate of hepatic fatty acid synthesis and the activities of hepatic fatty acid synthetase (FAS) and malic enzyme (ME). In all four experiments, glucose-6-phosphate dehydrogenase (G6PD) activity was significantly depressed by C18:2 and C18:3. C18:1 produced an intermediate rate of in vitro liver fatty acid synthesis, but exerted no significant effect on hepatic lipogenic enzyme activities. Adding C16:0 or C18:0 to the FF-diet had no depressive effect on hepatic fatty acid synthesis, but C18:0 supplementation was associated with a significant increase in hepatic FAS, C6PD and ME activities. Neither unsaturated nor saturated fatty acids affected adipose tissue FAS, G6PD or ME activities or rates of fatty acid synthesis. The lack of influence of C16:0 and C18:0 may have been partially due to their poor absorbability. Therefore, in experiment 4 a level of 7% C16:0 supplementation was compared to 3% C18:2 or C18:3. This resulted in comparable amounts of fatty acid absorbed. Both C18:2 and C18:3 addition to the FF-diet were equally effective in significantly depressing in vivo hepatic fatty acid synthesis, and FAS, G6PD and ME activities by more than 50%. C16:0 had no suppressive action on liver fatty acid synthesis or related enzyme activities. Again adipose tissue lipogenesis remained unchanged by dietary fat treatment. These data clearly demonstrate that C18:2 and C18:3 specifically inhibit rat liver fatty acid synthesis, independent of carbohydrate intake. Under these conditions adipose tissue lipogenesis was unaffected by low levels of dietary fat regardless of the degree of unsaturation.

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