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PubMed1994

Stearic acid metabolism and atherogenesis: history.

Studies conducted in dogs, rats, and hamsters show that stearic acid or stearic acid-rich glycerides are absorbed less efficiently than are lauric, myristic, and palmitic acids or their triglycerides. This observation may explain in part why stearic acid is less cholesterolemic than saturated fatty acids of shorter chain length. In rabbits, cocoa butter or other fats rich in stearic acid are less atherogenic than other saturated fatty acids. This finding is true for both cholesterol-containing and cholesterol-free diets.

Absorption↗
PubMed1997

Stearic acid, trans fatty acids, and dairy fat: effects on serum and lipoprotein lipids, apolipoproteins, lipoprotein(a), and lipid transfer proteins in healthy subjects.

To compare the effects on serum lipoproteins of stearic acid, trans fatty acids, and dairy fat, 80 healthy subjects consumed a dairy fat-based (baseline) diet for 5 wk, then an experimental diet high in either trans fatty acids (8.7% of energy; n = 40) or stearic acid (9.3% of energy; n = 40) for another 5 wk. All diets provided 32.2-33.9% of energy as fat, 14.6-15.8% as saturated plus trans fatty acids, 11.4-12.5% as cis-monounsaturated fatty acids, 2.9-3.5% as polyunsaturated fatty acids, and 200-221 mg cholesterol/10 MJ. Compared with the dairy fat diet, stearic acid and trans fatty acids decreased serum total cholesterol concentrations similarly (by 13% and 12%, respectively, P < 0.001) but the trans fatty acid diet decreased HDL cholesterol (17%) and apolipoprotein (apo) A-I (15%) significantly more than did the stearic acid diet (11% and 12%, respectively). Stearic acid but not trans fatty acids reduced concentrations of LDL cholesterol and apo B significantly (P < 0.001). The trans fatty acid diet increased the ratio of LDL to HDL cholesterol (19%) and of apo B to apo A-I (16%) more than did the dairy fat diet (P < 0.001) but the stearic acid diet had no effect. Lipoprotein(a) concentrations increased with both experimental diets, significantly more with trans fatty acids (30%) than with stearic acid (10%). In conclusion, high amounts of trans fatty acids had more adverse effects on lipoproteins than did equal amounts of stearic acid and dairy fat. Stearic acid reduced LDL cholesterol, did not affect the ratio of LDL to HDL cholesterol, and increased lipoprotein(a), although to a lesser extent than did trans fatty acids. Dietary fats low in both saturated fatty acids and trans fatty acids should be favored.

Adult↗
PubMed1995

Plasma cholesterol-predictive equations demonstrate that stearic acid is neutral and monounsaturated fatty acids are hypocholesterolemic.

In the present study we used regression analyses to evaluate the effects of stearic acid (18:0) on total cholesterol (TC), low-density-lipoprotein-cholesterol (LDL-C), and high-density-lipoprotein-cholesterol (HDL-C) concentrations (mmol/L). Using data from 18 articles, we developed the following predictive equations (monounsaturated fatty acids, MUFAs; polyunsaturated fatty acids, PUFAs): delta TC = 0.0522 delta 12:0-16:0 - 0.0008 delta 18:0 - 0.0124 delta MUFA - 0.0248 delta PUFA; delta LDL-C = 0.0378 delta 12:0-16:0 + 0.0018 delta 18:0 - 0.0178 delta MUFA - 0.0248 delta PUFA; delta HDL-C = 0.0160 delta 12:0-16:0 - 0.0016 delta 18:0 + 0.0101 delta MUFA + 0.0062 delta PUFA. Our analyses revealed that unlike the other long-chain saturated fatty acids (SFAs), stearic acid had no effect on TC and lipoprotein cholesterol concentrations in men and women. MUFAs elicited an independent hypocholesterolemic effect that we believe is due to the small amount of 12:0-16:0 in the experimental diets evaluated. The observation that stearic acid has unique effects on TC, LDL-C, and HDL-C provides additional compelling evidence that it be distinguished from the other major SFAs in blood cholesterol predictive equations.

Adult↗
PubMed1992

Effects of stearic acid and beef tallow on iron utilization by the rat.

Two experiments were done in which anemic rats were fed diets containing safflower oil or stearic acid and low (10 ppm) or adequate (39-42 ppm) iron. Diets were 24% fat by weight. In the stearic acid diets, 2% (Experiment 1) or 4% (Experiment 2) of the fat was supplied by safflower oil to satisfy essential fatty acid requirements. Repletion of hemoglobin, hematocrit, and liver iron was assessed. Compared with safflower oil in both experiments, stearic acid had a significant positive effect (P less than 0.0001) on repletion of hemoglobin (Hb), hematocrit (Hct), and liver iron concentration; the effect on Hb and Hct was most pronounced when dietary iron was low. When expressed as g Hb/mg Fe intake, Hb repletion was affected by a significant interaction between fat and Fe (P less than 0.002) and was greatest in rats fed low iron stearic acid diets. In a third experiment, rats were fed low dietary iron and 24% safflower oil, 20% stearic acid + 4% safflower oil, 3.2% stearic acid + 20.8% safflower oil, or 20% beef tallow + 4% safflower oil. The 20% beef tallow provided 3.2% stearic acid in the total diet. The response of Hb and Hct were similar to those in the first two experiments for rats fed safflower oil or stearic acid. Rats fed beef tallow had significantly greater (P less than 0.05) Hb and Hct repletion than did rats fed safflower oil, although the degree of repletion was less than that observed in rats fed 20% stearic acid. There was no difference in iron repletion of rats fed 3.2% stearic acid and rats fed beef tallow. We conclude that stearic acid enhances iron utilization by rats.

Animals↗
PubMedDate not supplied

Incorporation of 14C stearic acid in lens organ culture.

14C stearic acid was incubated in organ culture of rabbit lens for 6, 12 and 20 hours. Stearic acid did penetrate the lens and was incorporated into triacyl-glycerides and phospholipids. It also served as a carbon source for cholesterol synthesis. Individual fatty acids were isolated and radioactivity measurements were made. Incorporation of label was found in C12:0, C14:0 and C16:0 fatty acids, indicating de novo synthesis in the lens; incorporation was found in C16:1 and C18:1, indicating delta 9 desaturase activity, and incorporation was found in the fatty acids of 20 carbons or longer, indicating the presence of a fatty acid elongation system in the lens.

Animals↗
PubMed1985

Biphasic liberation of arachidonic and stearic acids during cerebral ischemia.

The mode of free fatty acid (FFA) liberation from the mouse brain during ischemia was investigated at various times after decapitation and under nizofenone treatment. Normal nonischemic brain FFAs consist mainly of palmitic acid (16:0), stearic acid (18:0), and oleic acid (18:1) with smaller amounts of arachidonic acid (20:4), docosahexaenoic acid (22:6), and others. Postdecapitative ischemia induced a rapid, biphasic release of 20:4 after a short lag of less than 30 s. The first phase showed a rapid 6.4-fold increase within 1 min of decapitation, followed by the second phase involving a slow release at less than one-fifth the rate of the first phase and lasting for at least 10 min. A similar, but not so marked, biphasic liberation was observed with 18:0. However, all of the other fatty acids (16:0, 18:1, 22:6, and others) were released only in a single phase at a slow rate. The time course for the rapid and specific liberation of 20:4 coincided with the time course for the decrease in brain ATP concentration during ischemia. Pretreatment of the animals with nizofenone resulted in a marked suppression of both FFA liberation and ATP depletion during ischemia. This suppression was particularly noteworthy with 20:4 and 18:0. The present study indicates that there is a specific and rapid liberation of 20:4 and 18:0 in a very early stage of ischemia and that this liberation seems to depend on availability of ATP in the brain. The physiological role of this transient 20:4 liberation during ischemia is discussed.

Adenosine Triphosphate↗
PubMed2005

Molecular analysis of the high stearic acid content in sunflower mutant CAS-14.

Increasing the stearic acid content to improve sunflower (Helianthus annuus L.) oil quality is a desirable breeding objective for food-processing applications. CAS-14 is a sunflower mutant line with a high stearic acid content in its seed oil (>35% vs. <6% in currently grown sunflower hybrids), which is controlled by the Es3 gene. However, the expression of the high stearic acid character in CAS-14 is strongly influenced by temperature during seed maturation and it is not uniform along the seed. The objectives of this study were (1) to identify PCR-based molecular markers linked to the Es3 gene from CAS-14, (2) to map this gene on the sunflower genetic map, and (3) to characterize the interaction between CAS-14 and CAS-3, a sunflower high stearic acid (about 26%) mutant line with the Es1 and Es2 genes determining this trait. Two F2 mapping populations were developed from crosses between CAS-14 and P21, a nuclear male sterile line with the Ms11 gene controlling this character, and between CAS-14 and CAS-3. One hundred and thirty-three individuals from P21xCAS-14, and 164 individuals from CAS-3xCAS-14 were phenotyped in F2 and F3 seed generations for fatty acid composition using gas-liquid chromatography, and they were then genotyped with microsatellite [simple sequence repeat (SSR)] and insertion-deletion (INDEL) markers. Bulk segregant analysis in the P21xCAS-14 population identified two markers on LG 8 putatively linked to Es3. A large linkage group was identified using additional markers mapping to LG 8. Es3 mapped to the distal half of LG 8 and was flanked by the SSR markers ORS243 and ORS1161 at genetic distances of 0.5, and 3.9 cM, respectively. The Ms11 gene was also mapped to LG 8 and genetic distance between this gene and Es3 was found to be 7.4 cM. In the CAS-3xCAS-14 population, two QTLs were identified on LG 1 and LG 8, which underlie the Es1 gene from CAS-3 and the Es3 gene from CAS-14, respectively. A significant epistatic interaction between these two QTLs was found. Results from this study provided a basis for determining CAS-14 efficient breeding strategies.

Breeding↗
PubMed1978

The binding isotherms for the interaction of 5-doxyl stearic acid with bovine and human albumin.

Binding isotherms for the interaction of 5-doxyl stearic acid with bovine and human albumin are reported. The critical micelle concentration (CMC) and the limiting solubility of 5-doxyl stearic acid were determined using the electron spin resonance (ESR)-spin label method. The CMC and the limiting solubility of this spin-label stearic acid in saline-phosphate buffer are 3.5 x 10(-5) M and 2 x 10(-4) M, respectively. We found no ESR line width evidence for pre-association of the spin-label stearate below the CMC. Maximum binding of the spin-label stearate to both bovine and human albumin occurs before micelle formation. The binding isotherm for spin-label stearic acid interaction with bovine albumin is in agreement with data obtained by others using [1-(14)C]stearic acid. For human albumin, comparison is difficult since previous data obtained with [1-(14)C]stearic acid vary widely. Comparison of the ESR 2T(||) values (the splitting between low and high field extremes, a measure of the degree of immobilization of protein-bound spin-label stearate) for bovine and human albumin indicates a greater immobilization of the spin-label molecules bound to human albumin. The binding data indicate that complexes are formed with bound spin-label stearate/albumin ratios of at least 18. The computed equilibrium constants for both bovine and human albumin indicate that the first seven spin-label molecules are tightly bound, log K > 5.0. The species predicted to form in solution by these equilibrium constants are reported.

Electron Spin Resonance Spectroscopy↗
PubMed1989

Intestinal absorption of stearic acid after consumption of high fat meals in humans.

The intestinal absorption of stearic acid (18:0), relative to other fatty acids, was evaluated in a group of 10 normal volunteers. Subjects were fed two types of high fat meals; one contained a relatively high content of stearic acid and the other a relatively low content. Plasma chylomicrons were isolated at 2, 4, 6 and 8 h after ingestion of the meals. Fatty acid patterns of chylomicron lipids were determined, and relative intestinal absorption rates of each fatty acid were estimated by comparing the fatty acid composition of chylomicron lipids with that of the fat in the meals. Overall, for both meals the fatty acid pattern of chylomicron lipids was very similar to that of ingested fat. Percentages of palmitic acid (16:0) and stearic acid, relative to other fatty acids, were only slightly lower in chylomicron lipids than in the meal fat. These data suggest that intestinal absorbability of stearic acid is similar to that of palmitic acid, and both saturated fatty acids appear to be absorbed almost as well as oleic acid (16:1).

Adult↗
PubMed2003

Stearic acid facilitates hippocampal neurotransmission by enhancing nicotinic ACh receptor responses via a PKC pathway.

Of a variety of saturated free fatty acids examined here, those with less than 20 hydrocarbon potentiated responses through Torpedo ACh receptors expressed in Xenopus oocytes, and the maximal effect was obtained with stearic acid (C18:0) at 10 microM (168+/-25% of basal levels 10 min after 10-min treatment). Stearic aid (10 microM) also potentiated alpha7 nicotinic ACh receptor responses, being evident 110 min after 10-min treatment (219+/-18% of basal levels), and the potentiation was inhibited by GF109203X, a selective inhibitor of protein kinase C (PKC). In the PKC assay using a reversed-phase HPLC, stearic acid (10 microM) enhanced PKC-epsilon activity approximately twice as much as the activity in the absence of stearic acid. Stearic acid (10 microM) induced a long-lasting facilitation of neurotransmission in the dentate gyrus of rat hippocampal slices, and the facilitation was inhibited by GF109203X or alpha-bungarotoxin, an inhibitor of alpha7 receptors. The results presented here suggest that stearic acid facilitates hippocampal neurotransmission by enhancing alpha7 receptor responses via a PKC pathway.

Animals↗