Selective use of palmitic acid over stearic acid for synthesis of phosphatidylcholine and phosphatidylglycerol in lung

The incorporation of [³H]palmitic acid and [¹⁴C]stearic acid into phospholipids in rabbit lung tissue was studied. Under equal molar concentrations of palmitate and stearate, palmitate was incorporated to the 1- and 2-positions of phosphatidylcholine (PC) and phosphatidylglycerol (PG) 2–3 times more than stearate. By contrast, palmitate was 30% less than stearate in phosphatidylethanolamine, phosphatidylinositol and phosphatidylserine. These results suggest that preferential utilization of palmitate over stearate, rather than substrate availability, determines the high content of palmitoyl at the 1- and 2-positions of PC and PG in lung.     

Regulation of stearoyl-CoA desaturase expression

Stearoyl-CoA desaturase (SCD) is a regulatory enzyme in lipogenesis, catalyzing the rate-limiting step in the overall de novo synthesis of monousaturated FA, mainly oleate and palmitoleate from stearoyl- and palmitoyl-CoA, respectively. Oleate and palmitoleate are the major monounsaturated FA of membrane phospholipids, TG, wax esters, cholesterol esters, and alkyldiacylglycerol. Several SCD gene isoforms (SCD1, SCD2, SCD3, and SCD4) exist in mice, and two have been characterized in humans. SCD1 gene expression in liver cells is regulated by numerous stimuli including diet and hormones. We are interested in why SCD is such a highly regulated enzyme even though oleate, the major product of this enzyme, is one of the most abundant FA in the diet and is therefore readily available. Dietary oleate is also well known for its TG-lowering effects and, as a major component of olive oil, is expected to have beneficial effects. However, high SCD activity has been implicated in diabetes, obesity, atherosclerosis, and cancer in several animal models; therefore, the role that de novo oleate plays in these disease states has to be carefully evaluated. By using SCD1-/-mice, which are deficient in tissue oleate, we begin to learn more about the physiological role of SCD gene expression and oleate in normal and disease states.     

Dietary cholesterol modulates Δ6 and Δ9 desaturase mRNAs and enzymatic activity in rats fed a low-EFA diet

The effects of a 1% addition of cholesterol to a diet low in EFA on FA desaturases were examined. The administration of cholesterol markedly increased the esterified cholesterol content in microsomes and total liver lipids from the first day, whereas the proportion of free cholesterol remained unaltered throughout the treatment. An excellent homeostasis in the free cholesterol content was apparently evoked by the acyl-CoA cholesterol acyltransferase. The cholesterol esters were mainly oleate, palmitate, and stearate, and the addition of cholesterol increased the relative proportions of cholesterol palmitoleate and oleate. The addition of cholesterol to a low-EFA diet induced, as in animals fed a high-FFA diet, a marked increase in liver stearoyl-CoA desaturase-1 mRNA and enzyme activity. This increased activity apparently evoked a similar enhancement of palmitoleic and oleic acids in total and microsomal liver lipids. The cholesterol-rich diet depressed the liver Δ6 and Δ5 desaturase activity. However, the abundance of Δ6 desaturase mRNA was not modified throughout the treatment. This indicates that the depressive effect is evoked at a step beyond that controlled by the mRNA level. The depression of both enzymatic activities was consistent with the decrease in the percentages of arachidonic acid and DHA in total and microsomal liver lipids. Taken together, these results indicate that through its modulating effect on the desaturases, dietary cholesterol may lead an animal or humaan fed low-EFA diet to a true deficiency by the decreased synthesis of the highly polyunsaturated acids derived from linoleic and α-linolenic acids.     

<Emphasis Type="Italic">In vitro</Emphasis> effects of fat,FA, and cholesterol on sphingomyelin hydrolysis induced by rat intestinal alkaline sphingomyelinase

Dietary sphingomyelin (SM) may have regulatory effects on cell proliferation and tumorigenesis in the colon. Alkaline sphingomyelinase (SMase) is the major enzyme responsible for hydrolysis of SM in the gut. Previously we purified the enzyme and showed that the presence of glycerophospholipids inhibited SM hydrolysis induced by alkaline SMase in vitro. In the present work, we studied the effects of TG, DG, FA, ceramide, and cholesterol on SM hydrolysis catalyzed by purified alkaline SMase. The results showed that both TG (triolein and tristearin) and DG (1,2-dioleoyl-sn-glycerol and 1,2-distearoyl-rac-glycerol) inhibited the activity of alkaline SMase. 1-Mono-oleoyl-rac-glycerol, 1-monostearoyl-rac-glycerol, stearic acid, oleic acid, linoleic acid, linolenic acid, and arachidonic acid stimulated the activity of alkaline SMase at 0.4–0.8 mM concentrations but inhibited the enzyme at higher concentrations. There was no difference between the effects induced by saturated and unsaturated FA. A short-chain FA such as lauric acid had a stronger stimulatory effect at low concentrations and weaker inhibitory effect at high concentrations than long-chain FA. Choosing linoleic acid as an example, we found that FA had similar effects on both alkaline SMase and neutral SMase. Cholesterol and ceramide when mixed with FA to increase its solubility in bile salt micelles inhibited SMase activity. In conclusion, glycerides, FA, ceramide, and cholesterol influence SM hydrolysis catalyzed by intestinal alkaline SMase. The presence of lipids in the diet may thus influence the course of SM digestion in the gut and thereby the exposure of colon to SM metabolites.     

Triglyceride composition of bovine milk fat with elevated levels of linoleic acid

The effect of increasing the linoleic acid (18∶2) content of milk fat on the composition and structure of the triglycerides (TG) was investigated. Protected sunflower seed supplement was added to the diet of a cow grazing on pasture, and the structure and composition of the milk fat compared with the milk fat from its monozygous twin which had been fed a control diet. The relative proportions of TG fractions of high, medium, and low molecular weight in the milk fat with elevated levels of 18∶2 (15.5% 18∶2) were 43.0, 19.5, and 37.5 moles %, respectively, compared with 36.1, 19.7, and 44.2 moles %, respectively, in the milk fat from the cow fed the control diet. Separation of these three TG fractions of each milk fat into TG classes with different levels of unsaturation showed that the milk fat with elevated levels of 18∶2 contained higher proportions of diene, triene, and tetraene TG and correspondingly lower proportions of saturated and, to a lesser extent, monoene TG. The saturated and monoene TG from the two milk fats had similar fatty acid compositions. However, the diene TG of the 18∶2-rich milk fat included high proportions of the combination of 18∶2 with two saturated fatty acids (FA) which are minor constituents of normal milk fats. Likewise, the triene TG reflected the presence of 18∶2 in combination with 18∶1 and a saturated FA.     

Effects of stearic acid on plasma lipid and lipoproteins in humans

More than 40 years ago, saturated FA with 12, 14, and 16 carbon atoms (lauric acid, myristic acid, and palmitic acid) were demonstrated to be “hypercholesterolemic saturated FA.” It was further concluded that the serum total cholesterol level would hardly be changed by isocaloric replacement of stearic acid (18∶0) by oleic acid (cis-18∶1n−9) or carbohydrates. These earlier studies did not address the effects of the various FA on the serum lipoprotein profile. Later studies found that the hypercholesterolemic saturated FA increase serum total cholesterol levels by raising concentrations of both the atherogenic LDL and the antiatherogenic HDL. Consequently, the ratio of total to HDL cholesterol will hardly change when carbohydrates replace these saturated FA. Compared with other saturated FA, stearic acid lowers LDL cholesterol. Studies on the effects on HDL cholesterol are less conclusive. In some, the effects on HDL cholesterol were comparable to those of palmitic acid, oleic acid, and linoleic acid, whereas in others a decrease was observed. This may suggest that in this respect the source of stearic acid is of importance, which needs however further study. From all these studies, however, it can be concluded that stearic acid may decrease the ratio of total to HDL cholesterol slightly when compared with palmitic or myristic acid. Without doubt, the effects of stearic acid are more favorable than those of trans monounsaturated FA.     

Down-Regulation of Hepatic Stearoyl-CoA Desaturase-1 Expression by Fucoxanthin via Leptin Signaling in Diabetic/Obese KK-A y Mice

Stearoyl-coenzyme A desaturase-1 (SCD1) is a rate-limiting enzyme that catalyzes the biosynthesis of monounsaturated fatty acids from saturated fatty acids. Recently, SCD1 down-regulation has been implicated in the prevention of obesity, and the improvement of insulin and leptin sensitivity. In this study, we examined the effect of fucoxanthin, a marine carotenoid, on hepatic SCD1 in obese mouse models of hyperleptinemia KK-A ^y and leptin-deficiency ob/ob. In KK-A ^y mice, providing a diet containing 0.2 % fucoxanthin for 2 weeks markedly suppressed SCD1 mRNA and protein expressions in the liver. The fatty acid composition of liver lipids was also affected by an observed decrease in the ratio of oleic acid to stearic acid. Furthermore, serum leptin levels were significantly decreased in hyperleptinemia KK-A ^y mice after 2 weeks of fucoxanthin feeding. However, the suppressive effects of fucoxanthin on hepatic SCD1 and body weight gain were not observed in ob/ob mice. These results show that fucoxanthin down-regulates SCD1 expression and alters fatty acid composition of the liver via regulation of leptin signaling in hyperleptinemia KK-A ^y mice but not in leptin-deficient ob/ob mice.     

TG containing stearic acid,synthesized from coconut oil,exhibit lipidemic effects in rats similar to those of cocoa butter

Lipase-catalyzed interesterification was used to prepare structured TG from coconut oil TG by partially replacing some of the atherogenic saturated FA with stearic acid, which is known to have a neutral effect on lipid levels in the body. The level of stearic acid was increased from 4% in the native coconut oil to 40% in the structured lipids, with most of the stearic acid being incorporated into the sn−1 and sn−3 positions of TG. When structured lipids were fed to rats at a 10% level for a period of 60 d, a 15% decrease in total cholesterol and a 23% decrease in LDL cholesterol levels in the serum were observed when compared to those fed coconut oil. Similarly, the total and free cholesterol levels in the livers of the rats fed structured lipids were lowered by 31 and 36%, respectively, when compared to those fed coconut oil. The TG levels in the serum and in the liver showed decreases of 14 and 30%, respectively, in animals fed structured lipids. Rats fed cocoa butter and structured lipids having a similar amount of stearic acid had similar lipid levels in the serum and liver. These studies indicated that the atherogenic potential of coconut oil lipids can be reduced significantly by enriching them with stearic acid. This also changed the physical properties of coconut oil closer to those of cocoa butter as determined by DSC.     

Effect of five cysteine-containing compounds on three lipogenic enzymes in Balb/cA mice consuming a high saturated fat diet

The in vivo effects of N-acetyl cysteine (NAC), S-allyl cysteine, S-ethy cysteine (SEC), S-methyl cysteine (SMC), and S-propyl cysteine (SPC) against hyperlipidemia development and oxidation stress in Balb/cA mice consuming a high saturated fat diet were examined. The influence of these agents on plasma levels of glucose, insulin, uric acid, TG, cholesterol, and the activity of three lipogenic enzymes—glucose-6-phosphate dehydrogenase, malic enzyme, and FA synthase—was determined. All mice consumed the coconut oil-basd, high saturated fat diet, water, and cysteine or one of the five cysteine-containing compounds for 4 wk. The diet with 18% saturated fat significantly elevated the activity of three lipogenic enzymes and significantly increased TG and cholesterol biosynthesis in plasma and liver (P<0.05). When compared with the water and cysteine groups, the treatments from five cysteine-containing agents significantly reduced high saturated fat diet-increased malic enzyme and FA synthase activities, and significantly lowered TG levels in plasma and liver (P<0.05); however, only NAC, SAC, and SMC treatments significantly reduced cholesterol levels in plasma and liver (P<0.05). The five cysteine-containing agents significantly restored high saturated fat diet-decreased glutathione peroxidase (GPX) activity in liver (P<0.05); however, only SMC and SPC significantly restored GPX activity in heart and kidney (P<0.05). These agents also significantly improved high saturated fat diet-related hyperglycemia, hyperuricemia, and oxidation stress (P<0.05). These data support the hypothesis that these compounds are potential multiply-protective agents for hyperlipidemia prevention or therapy.     

The effect of methyl sterculate on oleic acid synthesis in the hen

The enzymic desaturation of saturated fatty acids to monoenes in animals and plants is inhibited by cyclopropene fatty acids, such as sterculic acid. Labeled acetic and stearic acids were administered to laying hens which had received methyl sterculate in the diet for long periods, and the incorporation of the label in the eggs and liver was studied. The egg was used as a “biological trap” to study the metabolism of the hen in relation to its diet. Maximum incorporation of label was observed in the third or fourth egg laid after administration of the labeled compound. Dietary methyl sterculate reduced the incorporation of stearic acid into egg yolk lipids, but the incorporation of acetate was not affected. The formation of oleic acid was inhibited by methyl sterculate irrespective of whether the prescursor was acetate or stearate acid. In laying hens receiving methyl sterculate for long periods, no evidence could be obtained for the biosynthesis of oleic acid by an alternative pathway which did not involve the desaturation of stearic acid. The validity of comparing the ratio of the specific activities of stearic acid and oleic acid in control birds with the corresponding ratio obtained for birds receiving methyl sterculate is questioned, because the sizes of the metabolic pools of the product and precursors may be quite different for the two groups of birds.     

Oviposition response ofLobesia botrana females to long-chain free fatty acids and esters from its eggs

Avoidance of occupied ovisposition sites supposes that females perceive information related to their own progency. Fatty acids identified from egg extracts have been reevaluated using a different extraction method, and we have investigated the dose-dependent oviposition response of European grape vine moths (Lobesia botrana) to myristic acid, palmitic acid, palmitoleic acid, stearic acid, oleic acid, linoleic acid, methyl palmitate, methyl oleate, and ethyl palmitate; all except ethyl palmitate have been identified from eggs ofL. botrana. A methylene dichloride extract of eggs fromL. botrana revealed the presence of saturated free fatty acids (myristic, palmitic, and stearic) and unsaturated acids (palmitoleic, oleic, linoleic, and linolenic) in amounts ranging from 3.9 ng/egg equivalent for myristic acid to 30 ng/egg equivalent for palmitic and oleic acids. The extract also contained traces of methyl palmitate and methyl stearate. The greatest avoidance indexes were observed in response to palmitic, palmitoleic, and oleic acids. All the other compounds tested caused weaker responses. A reduction in the number of eggs laid was observed when moths were exposed to each of the esters applied at 0.3 µg per application spot. Reduction in eggs laid was also observed at a 10-fold higher dose of oleic acid. The present results confirm that general and simple molecules can be involved in the regulation of oviposition site selection and that they may participate in chemical marking of the eggs.     

Freezing-point behavior of the ternary reciprocal salt pair system involving the cyclohexylamine and morpholine salts of stearic and palmitic acids

Summary Binary and quasi-binary freezing-point data have been obtained to establish the freezing-point diagram for the ternary reciprocal salt pair system involving cyclohexylamine stearate, cyclohexylamine palmitate, morpholine stearate, and morpholine palmitate. The compositions and freezing points of the ternary peritectic and eutectic mixtures have been determined. Cyclohexylamine palmitate and morpholine stearate are the “stable salt pair.” From the diagram it is possible to predict the freezing behavior of any molten mixture of these salts, including the temperature at which crystals of each component will appear on cooling, the yields of these crystals and the composition of the liquid phase at various temperatures, and the temperature at which maximum yields of crystals of the specific salts can be obtained. The data supply fundamental information in connection with the crystallization of mixed amine salts in the purification of palmitic and stearic acids. One of the laboratories of the Southern Utilization Research and Development Division, Agricultural Research Service, U. S. Department of Agriculture.     

The formation of phosphatidylinositol by acylation of 2-acyl-sn-glycero-3-phosphorylinositol in rat liver microsomes

The conversion of 2-acyl-sn-glycero-3-phosphorylinositol into phosphatidylinositol via acyl-CoA: 2-acyl-sn-glycero-3-phosphorylinositol acyltransferase activity was found to occur in rat liver microsomes. Over a wide range of conditions, stearic acid was preferred over palmitate by the acyltransferase when these acids were presented in mixtures as acyl-CoA derivatives. The potential importance of this enzyme activity for the entry of stearic acid into the 1-position of hepatic phosphatidylinositol is further supported by its greater preference for stearate relative to the acyl-CoA: 2-acyl-sn-glycero-3-phosphorylcholine acyltransferase under certain assay conditions.     

Lipid characterization of seed oils from high-palmitic,low-palmitoleic,and very high-stearic acid sunflower lines

Information obtained in recent years regarding the enzymes involved in FA synthesis can now be applied to develop novel sunflower lines by incorporating enzymes with specific characteristics into lines with a defined background. We have generated three highly saturated mutant lines in this way and characterized their FA content. The new high-palmitic, low-palmitoleic lines CAS-18 and CAS-25, the latter on a high-oleic background, have been selected from the high-stearic mutant CAS-3 by introducing a deficient stearic acid desaturase in a high-palmitic background from the previously developed mutant lines CAS-5 and CAS-12, respectively. As such, the desaturation of palmitic acid and the synthesis of palmitoleic acid and its derivatives (asclepic and palmitolinoleic acids) were reduced in these high-palmitic lines, increasing the stearic acid content. Likewise, introducing a FA thioesterase from a high-palmitic line (e.g., CAS-5) into the high-stearic CAS-3 increased the stearic acid content from 27 to 32% in the new high-stearic line CAS-31. As previously described in high-palmitic lines, high growth temperatures did not reduce the linoleic acid content of the oil. Furthermore, the FA composition of TAG, DAG, and phospholipids was modified in these lines. Besides a high degree of saturation, the TAG from these new vegetable oils have a low content of saturated FA in the sn-2 position. The α asymmetric coefficient obtained also indicates that the saturated FA are asymmetrically distributed within the TAG molecules. Indeed, the disaturated TAG content rose from 31.8 to 48.2%. These values of disaturated TAG are the highest to date in a temperate oilseed.     

Regulation by carbohydrate and clofibric acid of palmitoyl-CoA chain elongation in the liver of rats

Regulation of palmitoyl-CoA chain elongation (PCE) and its contribution to oleic acid formation were investigated in rat liver in comparison with stearoyl-CoA desaturase (SCD). Hepatic PCE activity was induced by the administration of 20% wt/vol glucose or fructose in the drinking water of normal rats. In streptozotocin-induced diabetic rats, the activities of both PCE and SCD were suppressed, and fructose, but not glucose, feeding caused an increase in the activities of both enzymes. Treatment of normal rats with clofibric acid in combination with carbohydrate further increased PCE, but not SCD, acitivity. FA analysis of hepatic lipids revealed that the proportion of oleic acid (18∶1n−9) increased upon administration of carbohydrate or clofibric acid. The treatment of rats with clofibric acid in combination with carbohydrate greatly increased the proportion of 18∶1n−9. A significant correlation was observed between PCE activity and the hepatic proportion of 18∶1n−9 (r ²=0.874, Po0.01), whereas the relationship between SCD activity and the proportion of 18∶1n−9 was not significant (r ²=0.552, P>0.05). Taken together, these results suggest that carbohydrate induces PCE as well as SCD activity to increase the hepatic 18∶1 content in rat liver, and the increased PCE activity seems to be responsible for the further increase in 18∶1n−9 when carbohydrate is administered in combination with clofibric acid. FA are designated by the number of carbon atoms and double bonds     

Effects of conjugated linoleic acid and troglitazone on lipid accumulation and composition in lean and Zucker diabetic fatty (fa/fa) rats

Dietary CLA has been shown to enhance glucose tolerance in several animal models, but in mice it induces insulin resistance and lipodystrophy. In this study, the effects of 2 wk of diet supplementation with either 1,5% CLA or 0.2% troglitazone (TZD), an insulin-sensitizing thiazolidinedione, on glucose tolerance, lipid accumulation, and composition of both lean and Zucker diabetic fatty (fa/fa; ZDF) rats were examined. Compared with lean rats, which maintained normal glucose tolerances after 2 wk of feeding regardless of diet, ZDF rats fed a control diet (CON) had significantly worsened glucose tolerance. ZDF rats fed CLA and TZD diets, however, maintained normal glucose tolerances. In contrast to the significantly elevated lipid levels in ZDF rats fed the CON diet, concentrations of plasma FFA and TG in ZDF rats fed CLA and TZD diets were normalized. A similar reduction of plasma lipid levels was observed in lean rats fed CLA and TZD compared with lean rats fed the CON diet. Although ZDF CON rats developed significant hepatic steatosis, both CLA-and TZD-fed rats had hepatic TG levels similar to those of lean rats. Both lean and ZDF rats fed the CLA diet had reduced adipose mass compared with respective genotype controls; however, TZD had no effect. Ratios of 16∶1/16∶0 and 18∶1/18∶0 FA, surrogate markers for stearoyl-CoA desaturase-1 (SCD-1) activity, were reduced in livers of ZDF rats fed CLA and TZD diets. These results show that, like TZD, CLA normalizes glucose tolerance and plasma lipids and also improves hepatic steatosis and FA composition in ZDF rats. The effects of CLA and TZD on hepatic lipid composition suggest that the effects of these two agents on glucose tolerance may be associated with a reduction in SCD-1.     

Stearic acid unlike shorter-chain saturated fatty acids is poorly utilized for triacylglycerol synthesis and β-oxidation in cultured rat hepatocytes

Utilization of stearate as compared to various saturated fatty acids for cholesterol and lipid synthesis and β-oxidation was determined in primary culture of rat hepatocytes. At 0.5 mmol/L in the medium, stearate (18:0) adequately solubilized by albumin was less inhibitory to cholesterol synthesis from [2-¹⁴C] acetate than myristate (14:0) and palmitate (16:0) (68% vs. 91 and 88% inhibition, respectively). The rate of incorporation into cholesterol from [1-¹⁴C] stearate (3.0±0.6 nmol/mg protein/4 h) was 37-, 1.8-, and 7.8-fold of that from myristate, palmitate, and oleate, respectively. Conversely, the rate of [1-¹⁴C] stearate incorporation into total glycerolipids was 88–90% lower than that of labeled palmitate, myristate, and oleate. The rate of [1-¹⁴C] stearate incorporation into triacylglycerol (3.6±0.4 nmol/mg protein/4 h) was 6–8% of that from myristate, palmitate, oleate, and linoleate. The rate of stearate incorporation into phospholipids was the lowest among tested fatty acids, whereas the rate of mono- and diacylglycerol synthesis was the highest with stearate treatment. The rate of β-oxidation as measured by CO₂ and acid soluble metabolite production was also the lowest with [1-¹⁴C] stearate treatment at 22.7 nmol/mg protein/4 h, which was 35–40% of those from other [1-¹⁴C] labeled fatty acids. A greater proportion of stearate than other fatty acids taken up by the hepatocytes remained free and was not metabolized. Clearly, stearate as compared to shorter-chain saturated fatty acids was less efficiently oxidized and esterified to triacylglycerol in cultured rat hepatocytes.     

Differential alteration of Δ9 and Δ6 desaturation of fatty acids in rat brain preparations in vitro

Developing rat brain has the capacity for either Δ9 or Δ6 desaturation of fatty acids. In liver, evidence supports the existence of separate enzymes for each reaction, but it is not known whether in brain Δ9 or Δ6 desaturation of saturated fatty acids involves distinct enzymes. We have used fatty acids, including the cyclopropene fatty acid, sterculic acid, to alter desaturation activities with substrates that are desaturated predominantly in the Δ9 position or in the Δ6 position. In addition, differential alteration of desaturation of plamitic acid, a substrate that can be desaturated in either the Δ9 or Δ6 positions by brain preparations from neonatal rats, was examined. Sterculate reduced Δ9 desaturation of palmitate 80–90% but reduced Δ6 desaturation only 35%. In contrast, linoleic acid preferentially reduced Δ6 desaturation of palmitate. Thus, Δ9 desaturation of saturated fatty acids appears to be catalyzed by an enzyme or enzyme site distinct from that for Δ6 desaturation. Accordingly, these activities may be independently regulated during crucial stages of brain development.     

Dehydroepiandrosterone alters phospholipid profiles in Zucker rat muscle tissue

Insulin-resistant muscle tissue contains low proportions of arachidonic acid (AA), and increased proportions of muscle AA correlate with improved insulin sensitivity. Dehydroepiandrosterone (DHEA) and AA, like the thiazolidinedione drugs that decrease insulin resistance (IR), are peroxisome proliferators. Long-chain fatty acids (FA) have been named the “one true” endogenous ligand for activating the peroxisome proliferator-activator receptor (PPAR), and DHEA has been named a “good candidate” as a naturally occurring indirect activator of PPAR. This study was conducted to determine DHEA’s effects on lipid profiles of skeletal and cardiac muscle in lean and obese Zucker rats (ZR), a model of IR, type 2 diabetes mellitus, and obesity. We hypothesize that DHEA may alter long-chain FA profiles in muscle tissue of obese rats such that they more closely resemble that of the lean. In our experiments we employed a DHEA and a pair-fed (PF) group (n=6) for 12 lean and 12 obese ZR. For 30 d, the diet of the two DHEA groups was supplemented with 0.6% DHEA; PF groups were given the average daily calories consumed by their corresponding treatment group. Hearts and gastrocnemius muscles were assayed for phospholipid (PL), free FA, and triglyceride (TG) FA profiles. The proportion of PL AA was significantly greater in both muscle types of lean compared to obese rats. Hearts from both DHEA groups had greater PL proportions of AA and less oleic (18∶1) acid than their PF controls. Likewise, 18∶1 proportions were significantly lower in the gastrocnemius; however, AA proportions were not significantly different. Similar phenotypic profile differences were observed in the TG fraction of both muscle types. There were no DHEA-related TG FA profile alterations.     

Influence of stearic acid on hemostatic risk factors in humans

Stearic acid has been claimed to be prothrombotic. Elevated plasma factor VII coagulant activity (FVIIc) may raise the risk of coronary thrombosis in the event of plaque rupture. Fibrinogen, an acute-phase protein, is necessary for normal blood clotting; however, elevated levels of fibrinogen increase the risk of coronary heart disease (CHD). Here I report the results of three controlled, human dietary intervention studies, which used a randomized crossover design to investigate the hemostatic effects of stearic acid-rich test diets in healthy young men. A diet high in stearic acid (shea butter) resulted in a 13% lower fasting plasma FVIIc than a high palmitic acid diet, and was 18% lower than a diet high in myristic and lauric acids (P=0.001) after 3 wk of intervention. The stearic acid-rich test fat increased plasma fibrinogen concentrations slightly compared with the myristic-lauric acid diet (P<0.01). When investigating the acute effects of fatty meals, those high in stearic acid (synthesized test fat) resulted in a smaller postprandial increase in FVII than those high in trans and oleic FA, indicating a smaller increase in activated FVII after ingesting stearic acid compared with fats high in monounsaturated FA, probably caused by lower postprandial lipemia. Thus, the present investigations did not find dietary stearic acid to be more thrombogenic, in either fasting effects compared with other longchain FA, or in acute effects compared with dietary unsaturated FA, including trans monounsaturated FA. The slightly increased effect on fasting plasma fibrinogen may be biologically insignificant, but it should be investigated further.