Biochemistry of unsaturated fatty acid isomers

Recognition that catalytic hydrogenation changes the configuration and position of double bonds and alters the physical properties of unsaturated fats prompted numerous early investigations on the bio-chemical effects of ldtrans isomers.” Recent research has provided data on positional isomer metabolism. Some aspects of fatty acid isomer metabolism are now reasonably well understood, but other issues are not resolved. Human and animal data have provided good evidence that isomers in partially hydrogenated oils are well adsorbed and incorporated into all organs and tissues. Analyses of human tissues also indicate that hydrogenated oils are the major source of fatty acid isomers in the US diet. Tissue composition data combined with isolated enzyme studies and isotope tracer experiments with whole organisms show unquestionably that structural differences between various fatty acid isomers influence specific biochemical transformations. Examples are differences in the reaction rates and/ or specificities of acyl transferase, lipase, desaturase and cholesteryl esterase/hydrolase for various positional fatty acid isomers. Isolated microsomes and mitochondria also have been used to identify dif-ferences in acyl CoA activation, oxidation, and elongation of posi-tional isomers. In addition, isotope tracer experiments show that preferential metabolism of individual positional isomers occurs in vivo. In vivo studies with hydrogenated vegetable oil diets containing adequate levels of linoleic acid produced no obvious physiological changes. Experiments with specific polyunsaturated isomers have produced changes in blood cell properties, pulmonary weight, lino-leic acid requirements and tissue lipid composition. These changes may be related to a number of factors such as membrane fluidity and permeability, cell function, synthesis of arachidonic acid, homo-gamma-linoleic acid or prostaglandins. Whether differences in the biochemistry of fatty acid isomers are desirable or undesirable and whether these differences contribute to long-term or subtle effects important to the etiology of atherosclerosis and cancer are not resolved. Presented at the 73rd AOCS annual meeting, Toronto, 1982.