Jacqueline Dupont

Food uses and health effects of corn oil.

This review of corn oil provides a scientific assessment of the current knowledge of its contribution to the American diet. Refined corn oil is composed of 99% triacylglycerols with polyunsaturated fatty acid (PUFA) 59%, monounsaturated fatty acid 24%, and saturated fatty acid (SFA) 13%. The PUFA is linoleic acid (C18:2n-6) primarily, with a small amount of linolenic acid (C18:3n-3) giving a n-6/n-3 ratio of 83. Corn oil contains a significant amount of ubiquinone and high amounts of alpha- and gamma-tocopherols (vitamin E) that protect it from oxidative rancidity. It has good sensory qualities for use as a salad and cooking oil. Corn oil is highly digestible and provides energy and essential fatty acids (EFA). Linoleic acid is a dietary essential that is necessary for integrity of the skin, cell membranes, the immune system, and for synthesis of icosanoids. Icosanoids are necessary for reproductive, cardiovascular, renal, and gastrointestinal functions and resistance to disease. Corn oil is a highly effective food oil for lowering serum cholesterol. Because of its low content of SFAs which raises cholesterol and its high content of PUFAs which lowers cholesterol, consumption of corn oil can replace SFAs with PUFAs, and the combination is more effective in lowering cholesterol than simple reduction of SFA. PUFA primarily lowers low-density-lipoprotein cholesterol (LDL-C) which is atherogenic. Research shows that PUFA has little effect on high-density-lipoprotein cholesterol (HDL-C) which is protective against atherosclerosis. PUFA generally improves the ratio of LDL-C to HDL-C. Studies in animals show that PUFA is required for the growth of cancers; the amount required is considered to be greater than that which satisfies the EFA requirement of the host. At this time there is no indication from epidemiological studies that PUFA intake is associated with increased risk of breast or colon cancer, which have been suggested to be promoted by high-fat diets in humans. Recommendations for minimum PUFA intake to prevent gross EFA deficiency are about 3% of energy (en%). Recommendations for prevention of heart disease are 8-10 en%. Consumption of PUFA in the United States is 5-7 en%. The use of corn oil to contribute to a PUFA intake of 10 en% in the diet would be beneficial to heart health. No single source of salad or cooking oil provides an optimum fatty acid (FA) composition. Many questions remain to be answered about the relation of FA composition of the diet to various physiological functions and disease processes.

Quantitative relationships between dietary linoleate and prostaglandin (Eicosanoid) biosynthesis

Essential fatty acid deficiency consistently depresses eicosanoid (prostaglandin E2, F2, and I2 and thromboxane) biosynthesis independent of sampling protocols. Tissue fatty acid analyses support the hypothesis that the decrease is due in part to depression of arachidonate and accumulation of eicosatrienoate (n−9). Research on the alteration of eicosanoid biosynthesis by dietary linoleate supplementation is reviewed extensively. Responses of whole blood, lung, liver and heart eicosanoid synthesis to feeding eight concentrations of dietary linoleate between 0 and 27 energy percent are reported. It is concluded that stimulation, depression and no change in eicosanoid production could be equally well documented as a response to linoleate supplementation. Evidence for the obvious mechanism that alterations in precursor fatty acid composition are a possible explanation is fragmentary and inconsistent. The appropriate sampling techniques appear not to be established at this time and most likely are species, gender and tissue specific.

Essential fatty acids and prostaglandins.

The World Health Organizations recommendation for dietary intake of essential fatty acids is 3% of energy (en%) of linoleate. Evidence from rat studies suggests that more than 3 en% is desirable for the regulation of eicosanoid metabolism. With such a low level of available linoleate, humans tend to synthesize more prostanoids than they do with 6% or more energy from linoleate. High rates of prostanoid synthesis probably are deleterious, so that the lower rate commensurate with 6-12 en% of linoleate probably is desirable. The amount of linoleate needed for normal function is influenced by the dietary content of other fatty acids, particularly saturated fats and those of the n-3 family. Vitamin E is necessary for normal metabolism of polyunsaturated fatty acids. In a diet providing sufficient available total energy with 30% as fat, the lower range of linoleate (6-8 en%) probably is sufficient if the saturated fatty acid content is 10% or less. With a greater proportion of saturated fatty acids, more linoleate is needed to maintain a polyunsaturated to saturated fatty acid ratio of 0.7 to 1.0. Some n-3 fatty acids probably are required, and more than a minimal amount may be beneficial. Current recommendations are for 0.5-1.0 en% in a diet containing 5-6 en% of linoleate.

Effects of low fat diets differing in degree of fat unsaturation on plasma lipids, lipoproteins, and apolipoproteins in adult men.

The effects of two low fat diets with differing ratios of polyunsaturated to saturated fatty acids (P/S) on blood lipids, lipoproteins (LP), and apolipoproteins (Apo) were studied in 23 adult men, 30-60 years old, using a crossover design. Both test diets had 25% fat calories with either a P/S of 0.3 (Diet 1) or a P/S of 1.0 (Diet 2) and equivalent amounts of cholesterol. The study consisted of four periods: a 5-week prestudy on self-selected diet (SS), two 6-week test diet periods followed by a second 5-week post-study period on the SS diet. When compared with the SS diet, Diet 2 lowered the mean plasma total cholesterol (TC) by about 20% (P less than 0.01). Low density lipoprotein (LDL) cholesterol was also decreased by about 18% by Diet 2 (P less than 0.01). The high P/S diet did not cause a change in total cholesterol in the high density lipoprotein (HDL) subclass2 (HDL2) when compared to the SS diet. Levels of triglycerides (TG) were slightly reduced in HDL2 but showed a greater reduction in HDL3 in both diets. Phospholipids (PL) were significantly reduced in HDL2 and in HDL3, but the reduction in HDL3 PL was not statistically significant. Apo A-I levels were not changed by either diet when compared with the SS diet, but Apo A-II levels of HDL2 and HDL3 were significantly decreased by the low fat diets, and there was no P/S effect. No other consistent changes in apoprotein levels occurred. Our data suggest that, in men with normal lipid levels, practical dietary changes involving a moderate increase in P/S from 0.3 to 1.0 in a low fat, low cholesterol diet do influence lipoprotein composition and apoprotein distribution in a short time. The reduction in cholesterol in total lipid composition and in LDL lipids which accompanied the reduction of dietary fat and cholesterol are considered to be beneficial.

Bio-oxidation of linoleic acid via methylmalonyl-CoA1,2

Unsaturated long-chain fatty acids are oxidized more rapidly than are saturated fatty acids of similar chain length in intact animals and isolated mitochondria. Gamma-oxidation of the 3-dodecenoic acid intermediate in beta-oxidation of oleate would yield propionate which is metabolized via methylmalonate.14C-labeled fatty acids were administered to intact rats, muscle homogenates and lysed mitochondria. Methylmalonate, succinate and CO2 were isolated and14C determined. Incorporation of U-14C-linoleate into methylmalonate in vitro was 20 times greater than from U-14C-palmitate. Rats fed 20% corn oil grew more slowly on B12 deficient than B12 sufficient diets. Biotin and vitamin B12 deficiencies were found to decrease the in vivo metabolism of linoleate. These data suggest that one pathway of linoleate oxidation has methylmalonate as an intermediate.

Effects of Dietary Fat on Eicosanoid Production in Normal Tissues

To assess the relationship between dietary fat and eicosanoid functions, it is necessary to review briefly the general effects of deprivation of essential fatty acids. Availability of sufficient linoleate (18∶2n−6) and alpha-linolenate (18∶3n−3) in the diet and storage of an abundant supply in adipose tissue was considered to be ubiquitous in the human population until some 20 years ago. At that time the introduction of total parenteral alimentation created situations which revealed the fallacy of assuming that if there were fat stores there was no need to consider fatty acid status. The absolute requirement for linoleate for infants was demonstrated (1,2) and the inability to use fat stores under various treatment regimens was made clear. Adults receiving hypertonic glucose and amino acids developed essential fatty acid deficiency (EFAD) symptoms within days (3,4). Furthermore, newborns were shown to be marginally deficient at birth and, without lipid alimentation, rapidly developed biochemical evidence of EFAD (5). The metabolic pathways involved and interpretation of the biochemical lesions are fully described in other publications (6,7).

Effects of dietary fatty acids on the activity of glucose transport in adipocytes

Abstract Lipid structure of plasma membrane plays an important role in regulating D-glucose transport in adipocytes. To investigate the effects of diet-induced alteration in cellular fatty acids on the activity of D-glucose transport in adipocytes, we fed rats iso-nutrient diets with high (20 energy% safflower oil) or low (2 energy% safflower oil plus 18 energy% beef tallow) safflower oil. After 31 days, adipocytes were isolated from epididymal fat pads using collagenase and incubated at 310°K (37°C) in KRB buffer containing 3% bovine serum albumin. Two-deoxyglucose transport into adipocytes was measured using an oil centrifugation method at 2, 5, and 10 minutes of incubation. The composition of fatty acids was analyzed in the fat pad and adipocyte incubation mixture by using gas chromatography. In the fat pad, fatty acids were composed of 61% linoleic, 18% each of palmitic and oleic, and 0.7% arachidonic acids in the high safflower oil group, and 56% oleic, 31% palmitic, 8% linoleic acids in the low safflower oil group. The compositions of dietary fatty acids were reflected directly in the composition of fatty acids in the fat pads and in the compositions of fatty acids released from isolated adipocytes. The high safflower oil diet significantly increased D-glucose transport in adipocytes compared with the low safflower oil diet group (8.66 vs. 6.31 nmol 2-deoxyglucose transport per 106 cells at 5-minute incubation). The results suggest that lipid composition in the tissue may have a regulatory effect on adipocyte glucose transport. Diet-induced high polyunsaturated fatty acids in the tissue facilitates carrier-mediated D-glucose transport in adipocytes.

Gender differences in prostacyclin and prostaglandin E2 synthesis by human endothelial cells.

The incidence of atherosclerosis and thrombosis is higher in males than in females. Gender differences in prostacyclin synthesis by rat aortic rings have been described. In this paper, sex differences in prostacyclin (PGI2, measured as 6-keto PGF1 alpha) and prostaglandin E2 (PGE2) synthesis by human endothelial cells isolated from the vein of umbilical cords are reported. Cells isolated from cords from male babies synthesized more prostacyclin and PGE2 than cells isolated from those from female babies when the cells were stimulated with 0.125 units of thrombin. The difference in PGI2 was eliminated by incubation with 0.5 units of thrombin. PGE2 synthesis was higher in males than in females using both 0.125 and 0.5 units of thrombin. Incubation of the cells with culture medium containing 20% heat inactivated plasma from either male or female subjects did not have an effect upon prostaglandin synthesis. Our results support previous evidence obtained using rat aortas and show a higher response of male cells to thrombin stimulation than that of female cells.

Bile Acids in Extrahepatic Tissues

Unequivocal physical identification of individual nonhepatic bile acids is lacking, though there is evidence of the presence of cholanoic acids in brain [1, 2], skeletal muscle, kidney, pancreas, and adipose tissues [2]. The presence of cholanoic acids in tissues raises the question of whether the compounds originated by local biosynthesis or by transfer from blood after synthesis in the liver, even though it has been stated that the liver is the sole site of bile acid formation [3] without adequate evidence.

Cholanoic acids and cholesterol 7-α-hydroxylase activity in human leucocytes

Abstract Evidence is presented for the identification of cholanoic acids and cholesterol 7α-hydroxylase activity in human leucocytes. Mononucleated cells contained most of the detectable cholanoic acids. Cholesterol 7α-hydroxylase activity was present only in the mononuclear cells. These data suggest that cholanoic acids in leucocytes may have originated by local biosynthesis. Because of their lipid solubilizing properties, the cholanoic acids might have a function in the phagocytic activity of leucocytes.