Zinc deficiency and activities of lipogenic and glycolytic enzymes in liver of rats fed coconut oil or linseed oil

In previous studies, zinc-deficient rats force-fed a diet with coconut oil as the major dietary fat developed a fatty liver, whereas zinc-deficient rats force-fed a diet with linseed oil did not. The present study was conducted to elucidate the reason for this phenomenon. In a bifactorial experiment, rats were fed zinc-adequate or zinc-deficient diets containing either a mixture of coconut oil (70 g/kg) and safflower oil (10 g/kg) (“coconut oil diet”) or linseed oil (80 g/kg) (“linseed oil diet”) as a source of dietary fat, and activities of lipogenic and glycolytic enzymes in liver were determined. In order to ensure adequate food intake, all the rats were force-fed. Zinc-deficient rats on the coconut oil diet developed a fatty liver, characterized by elevated levels of triglycerides with saturated and monounsaturated fatty acids. These rats also had markedly elevated activities of the lipogenic enzymes acetyl-CoA carboxylase, fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH), and citrate cleavage enzyme, whereas activities of malic enzyme and glycolytic enzymes were not different compared with zinc-adequate rats on the coconut oil diet. In contrast, rats receiving the linseed oil diet had similar triglyceride concentrations regardless of zinc status, and activities of lipogenic enzymes and glycolytic enzymes were not different between the two groups. Zinc-deficient rats fed either type of dietary fat exhibited statistically significant correlations between activities of FAS, G6PDH, 6PGDH and concentrations of saturated and monounsaturated fatty acids in liver. The concentrations of serum lipids were elevated in zinc-deficient rats fed either type of dietary fat. These results demonstrate that fatty liver in zinc-deficient rats on the coconut oil diet is caused by elevated activities of lipogenic enzymes, and not by disturbed lipid secretion from liver. Dietary linseed oil prevents both the elevation of lipogenic enzyme activity and fatty liver in zinc-deficient rats.     

The effect of dietary vitamin E supply and a moderately oxidized oil on activities of hepatic lipogenic enzymes in rats

Diets rich in polyunsaturated fatty acids (PUFA) are well known to suppress hepatic lipogenic enzymes compared to fat-free diets or diets rich in saturated fatty acids. However, the mechanism underlying suppression of lipogenic enzymes is not quite clear. The present study was undertaken to investigate whether lipid peroxidation products are involved in suppression of lipogenic enzymes. Therefore, an experiment with growing male rats assigned to six groups over a period of 40 d was carried out. Rats received semisynthetic diets containing 9.5% coconut oil and 0.5% fresh soybean oil (coconut oil diet, peroxide value 5.1 meq O₂/kg oil), 10% fresh soybean oil (fresh soybean oil diet, peroxide value 0.5 meq O₂/kg oil), or 10% thermally treated soybean oil (oxidized soybean oil diet, peroxide value 74 meq O₂/kg oil). To modify the antioxidant state of the rats, we varied the vitamin E supply (11 and 511 mg α-tocopherol equivalents per kg of diet) according to a bi-factorial design. Food intake and body weight gain were not influenced by dietary fat and vitamin E supply. Activities of hepatic lipogenic enzymes were markedly influenced by the dietary fat. Feeding either fresh or oxidized soybean oil diets markedly reduced activities of fatty acid synthase, (FAS), acetyl CoA-carboxylase, (AcCX), glucose-6-phosphate dehydrogenase, (G6PDH), 6-phosphogluconate dehydrogenase, and ATP citrate lyase (ACL) relative to feeding the coconut oil diet. Moreover, feeding oxidized soybean oil slightly, but significantly, lowered activities of FAS, AcCX, and ACL compared to feeding fresh soybean oil. Activities of hepatic lipogenic enzymes were reflected by concentrations of triglycerides in liver and plasma. Rats fed the coconut oil diet had markedly higher triglyceride concentrations in liver and plasma than rats consuming fresh or oxidized soybean oil diets, and rats fed oxidized soybean oil had lower concentrations than rats fed fresh soybean oil. The vitamin E supply of the rats markedly influenced concentrations of thiobarbituric acid-reactive substances in liver, but it did not influence activities of hepatic lipogenic enzymes. Because the vitamin E supply had no effect, and ingestion of an oxidized oil had only a minor effect, on activities of hepatic lipogenic enzymes, it is strongly suggested that neither exogenous nor endogenous lipid peroxidation products play a significant role in the suppression of hepatic lipogenic enzymes by diets rich in PUFA. Therefore, we assumed that dietary PUFA themselves are involved in regulatio of hepatic lipogenic enzymes. Nevertheless, the study shows that ingestion of oxidized oils, regardless of the vitamin E supply, also affects hepatic lipogenesis, and hence influences triglyceride levels in liver and plasma.     

Effect of fat and microflora on hepatic,small intestinal and colonic HMG CoA reductase,cytochrome P450 and cytochrome B5

High levels of dietary fat caused a significant reduction in HMG CoA reductase activity in the liver of germ-free rats whereas significantly elevated small intestinal enzyme activity was observed. Dietary fat had no significant effect on HMG CoA reductase activity in any tissue studied in the conventional rat. No significant change in colonic HMG CoA reductase activity was observed between any of the experimental groups. Rats fed a high-fat diet tended to exhibit higher cytochrome P₄₅₀ levels in all tissues studied, regardless of the presence of intestinal microflora.     

Dietary fats and energy levels differently affect tissue lipogenic enzyme activity in finishing pigs

The aim of the present study was to determine the relationship between high and low digestible energy levels (9.5 vs. 15.4 MJ ME/kg) and either tallow or soy oil supplementation (5%rpar; on lipogenic activities and fatty acid profile of the backfat tissue outer layer and liver tissue in finishing pigs. Twenty Large White pigs averaging 30 (initial) to 106 kg (final) live weight were allocated into four dietary groups and fed the diets ad libitum. The lipid content and fatty acid composition of the tissues were determined and glucose-6-phosphate dehydrogenase (G6PDH), malic enzyme (ME), and fatty acid synthase (FAS) activity were measured. Growth performance and carcass measurements were affected by the dietary energy levels but not by the fat sources. Lipid deposition rate of animals fed the low energy diets was lowered regardless whether tallow or soy oil was supplemented. Unlike lipid deposition, fatty acid profile was influenced by both dietary factors. Pigs fed the low energy diet supplemented with soy oil exhibited the lowest level of saturated (P<0.001), monounsaturated (P<0.001), and the highest level of polyenic fatty acids in the backfat, the opposite was the case for the pigs fed the high energy diet supplemented with beef tallow. The fatty acid profile of the adipose tissue of animals fed the other two diets were intermediate, but clear distinction of the profile due to diets was visible. Independent of dietary treatments, lipogenic activities were up to 10 times higher in the backfat than in the liver. G6PDH activity was higher (P<0.05) due to high energy diet, whereas the activities of ME and FAS were not affected. Animals fed the high energy diet either supplemented with tallow or soy oil exhibited higher ME activity lpar;P<0.05) in the backfat, without any effects on G6PDH activity. In contrast, dietary fat sources affected the FAS activity, with lower activity lpar;P<0.05) exhibited in the backfat of animals fed the soy oil diets. The present results indicate that dietary manipulation, which change the flux through the pathway of lipogenesis and pentose-phosphate must affect differently the activities of the involved enzymes. The effect of the dietary energy level was stronger and overwhelmed the inducing effect of the PUFA on the activities of the collateral enzymes. In contrast the immediately involved lipogenic enzyme FAS responded more to dietary PUFA stimulation than to the energy supply.     

Lipogenic enzyme activities in primary cultures of adult mouse hepatocytes

The effects of various unsaturated fatty acids such as oleic (18∶1n−9), linoleic (18∶2n−6) and arachidonic (20∶4n−6) on the activities of fatty acid synthetase (FAS), malic enzyme (ME), glucose-6-phosphate dehydrogenase (G6PDH) and 6-phosphogluconate dehydrogenase (6PGDH) all were determined in primary cultures of mouse hepatocytes. Activities of FAS and ME were found to decrease with time in culture regardless of whether hepatocyte donors were fed diets containing polyunsaturated fatty acid-free hydrogenated cottonseed oil (HCTO) or corn oil (CO). On the other hand, while G6PDH activity also declined in cultured hepatocytes obtained from HCTO-fed mice, the activity of this enzyme increased in cells cultured from CO-fed mice. 6PGDH activity was found to increase in hepatocytes obtained from both diet groups. Neither 18∶2 nor 20∶4 when added to media could alter FAS or ME activities compared with those observed with either 18∶1-containing or fatty acid-free media. Since lactic dehydrogenase activity and the rate of incorporation of [³H] leucine into FAS protein were unaltered with time in hepatocyte cultures, the decreased activities of FAS and ME cannot be attributed to a loss in cell viability during culture but rather appear to be specific for those enzymes which respond to diet hormones in vivo. Examination of the fatty acid contents of the cells after the culture period showed that the values for the ratios of 16∶0/16∶1 and of 18∶0/18∶1 were elevated when either 18∶2 or 20∶4 was added to the medium even though there was no evidence for elongation of the added 18∶2 or for 20∶4 being converted to 22∶4. This result suggest that Δ9-desaturase activity was inhibited by these polyunsaturated fatty acids and that conversion of 18∶2 to 20∶4 was not required for such action. The rate of synthesis determined by the relative rate of incorporation of [³H]leucine into FAS was two to five times higher in hepatocytes prepared from mice fed the HCTO diet than in hepatocytes from mice fed the CO diet. We have concluded that the mechanisms for long-term regulation may not be contained entirely within the liver.     

Dietary fat effects on hepatic lipid peroxidation and enzymes of H2O2 metabolism and NADPH Generation

The purpose of this study was to determine the effects of dietary fat quantity and fatty acid composition on hepatic H₂O₂-metabolizing systems, activities of NADPH-generating enzymes and lipid peroxidation. Onemonth-old male C57BL/6J mice were fed one of six diets: (i) 5% fat, rich in 18∶2n−6 fatty acid (5% N−6); (ii) 20% fat, rich in 18∶3n−3 (N−3); (iii) 20% fat, rich in 18∶2n−6 (N−6); (iv) 20% fat, rich in 18∶1n−9 (N−9); (v) 20% fat, rich in saturated fatty acids (SAT); and (vi) 20% fat, deficient in essential fatty acids (EFAD); for 11 wk. Comparisons between animal groups receiving different fat quantities showed that activities of glucose-6-phosphate dehydrogenase (G6PDH, EC 1.1.1.49) and malic enzyme (ME, EC 1.1.1.40) and the levels of conjugated dienes were significantly lower in the N−6 than in 5% N−6 group. Conversely, activities of catalase (CAT, EC 1.11.1.6) and seleniumglutathione peroxidase (SeGSHPx, EC 1.11.1.9) were higher in the N−6 than in 5% N−6 group. Among the five dietary groups receiving 20% fat but differing in fatty acid composition, CAT activity was lower in the N−9 group, SeGSHPx activity was lower in the EFAD group, and glutathione reductase (GSSGR, EC 1.6.4.2) activity was higher in the N−6 than in the N−3, N−9, SAT and EFAD groups. The EFAD group had much higher levels of total lipids and conjugated dienes, as well as activities of NADPH-generating enzymes, including G6PDH, ME and isocitrate dehydrogenase (EC 1.1.1.42), than the other four high-fat groups. The hepatic levels of malondialdehyde were not different among the five groups fed 20% fat. In the EFAD group, higher hepatic lipid content can be attributed to higher activities of NADPH-generating enzymes, and the elevation of conjugated diene levels may be related to increased oxygenation of 20∶−6 (Mead acid)via the lipoxygenase/cyclooxygenase pathway. In short, both dietary fat quantity and fatty acid composition selectively affected hepatic H₂O₂-metabolizing systems, activities of NADPH-generating enzymes and lipid peroxidation status.     

Transesterification of brazilian vegetable oils with methanol over ion-exchange resins

The transesterification of several Brazilian vegetable oils with methanol was carried out at 60°C in the presence of several ion-exchange resins having different structures. The vegetable oils used were from Babassu coconut, corn, palm, palm kernel, and soybean. The effect of the methanol/oil mole ratio and the influences of the structure of the ion-exchange resin and the type of vegetable oil used on the catalytic activity of the ionexchange resins were investigated. The resins used were Amberlyst 15, Amberlyst 31, Amberlyst 35, and Amberlyst 36. Amberlyst 15 produced the best results for the transesterification of vegetable oils. The methyl ester yield is higher for palm kernel oil and Babassu coconut oil than for soybean oil, probably owing to their higher content of shorter-chain FA. Therefore, it was shown that the catalytic activity of the resin depends on the FA composition of the vegetable oil employed.     

Composition of oil

International trade in palm oil has increased considerably over the last ten years, and so too has the trade in processed palm oil products, especially palm fractions. It is important to establish reliable purity criteria for palm oil, not only because of the commercial need to verify oil authenticity, but also to comply with foodstuff labelling legislation in many countries. Palm kernel and coconut oils both contain about 47% lauric acid. This gives the oils close similarities in physical and chemical properties. The oils do differ, however, and it is important to be able to distinguish between them. Purity problems can arise as a result of commingling of oils with one another, or as a result of fractionation perhaps coupled with subsequent blending. A research program jointly funded by the (U.K.) Ministry of Agriculture, Fisheries and Foods, the Federation of Oils, Fats & Seeds Associations Ltd (FOSFA International), and the Leatherhead Food RA, was established to study purity characteristics of the major edible vegetable oils. Forty-seven samples of crude palm oil were obtained from reliable sources, often plantation managers, together with five samples of palm olein and eight samples of palm stearin. Fifty-four palm kernel and 23 coconut oils were obtained in the laboratory from seed samples of known geographical origins and authenticities. These oil samples were analyzed for fatty acid, triglyceride, sterol and tocopherol compositions; the melting properties were also determined, and in the case of palm oil the compositions of the acids at the triglyceride 2-positions were measured. Compositional ranges will be presented for the different geographical production areas in each case and related to existing data, e.g., of PORIM and Codex. An initial statistical analysis of the results has shown that a combination of values from the carbon number analysis differentiates palm kernel and coconut oils, and can be used to decide on the proportion of each in a blend. In the case of palm oil samples suspected to be contaminated with palm fractions, it was found useful to plot melting point against iodine value, and to compute the product of the C48 triglyceride content and the palmitic acid enrichment factor.     

应对月桂油的短缺

随着油脂化工生产的扩张,价格和基本原材料的获得是其成功的关键。月桂油（棕榈仁油和椰子油）对于油脂化学品的需求而言,在价格方面是最敏感的油品。目前月桂油主要用于食品方面,因此,油脂化工需求的增加必然导致月桂油的供应面临困难。月桂油的供应取决于椰子油和棕榈仁油的产量。油棕的产油率比椰棕高。很明显,将来月桂油供应主要取决于棕榈仁油生产的增加,这是棕榈油产量提高的结果。因此,为了提供充足的月桂油以满足油脂化学工业的需要,其用于食用方面的量将不得不减少。     

Palmöl und Palmkernöl

Palm Oil and Palm Kernel Oil Adulteration of palm oil with palm stearin can be recognized by examining the ration of the triglycerides PPP to MOP, which lies in pure palm oil between 3.5 and 4.5 and is elevated in the case of adulteration. The content of palmitic acid and the solid fat content are additional indications. Adulteration of coconut and palm kernal oils with palm kernel olein is best recognized by measuring the iodine number (which is max. 11 for coconut oil and 19 for palm kernel oil) and also by the content of stearic, oleic and linoleic acids, the sum of which should not exceed 11.5% for coconut oil and 22% for palm kernel oil respectively. The content of triglycerides with carbon number 46 to 54 may additionally be used.     

Cholesterol and fatty acid synthesis in swine

In incubation studies with swine tissue slices, acetate-1-¹⁴C or glucose-U-¹⁴C as substrates were incorporated more readily into fatty acids and cholesterol in adipose tissue than other tissues tested. Cholesterol and fatty acid synthesizing activity was substantial in the small intestine. When acetate was available, liver, small intestine, and adipose tissue were important sites for cholesterol synthesis. Heart and aortic tissue had marginal levels of cholesterol synthesizing ability. Lipogenesis in adult swine liver, heart, and aortic tissue was extremely low. As in tissue slices, incorporation of acetyl-1-¹⁴C CoA into fatty acids by adipose homogenates indicated high lipogenic activity. Subcellular fractionations of heart and aortic tissue indicated that the heart microsomal fraction had the highest lipogenic activity as measured by the incorporation of acetyl-1-¹⁴C CoA into fatty acids. In adult swine adipose tissue, the incorporation of glucose-U-¹⁴C into fatty acid was higher than its incorporation into glyceride-glycerol. The synthesis of glyceride-glycerol from glucose-U-¹⁴C or acetate-1-¹⁴C in liver was higher than for fatty acid synthesis. The activity of acetyl CoA carboxylase, fatty acid synthetase, citrate cleavage enzyme, nicotinamide adenine dinucleotide phosphate-malate dehydrogenase, glucose-6-phosphate dehydrogenase, and 6-phosphogluconate dehydrogenase was considerably higher in adipose tissue than in other tissues tested, paralleling its high lipogenic capacity. A preliminary report of this paper was given at the AOCS 66th Annual Spring Meeting, Dallas, Texas, April 30, 1975, Abstr. No. 109. In partial fulfillment of the requirement for the PhD degree in Nutritional Sciences at the University of Illinois at Urbana-Champaign.     

An enzymatic protective mechanism against lipid peroxidation damage to lungs of ozone-exposed rats

The effects of whole animal exposure to ozone and of dietary α-tocopherol on the occurrence in rat lung of lipid peroxidation and alteration of the activity of enzymes important in detoxification of lipid peroxides were studied. Exposure to 0.7 and 0.8 ppm ozone continuously for 5 and 7 days, respectively, significantly elevated the concentration of TBA reactants, primarily malonaldehyde, produced by lipid peroxidation, as well as the activities of glutathione (GSH) peroxidase, GSH reductase and glucose-6-phosphate (G-6-P) dehydrogenase. As a logarithmic function of dietary α-tocopherol (0, 10.5, 45, 150 and 1500 mg/kg), the increase in formation of malonaldehyde and the increase in activities of GSH peroxidase and G-6-P dehydrogenase were partially inhibited. The activity of GSH reductase was not affected by dietary α-tocopherol. The concentration of malonaldehyde and the activity of GSH peroxidase in lung were linearly correlated (p<0.001). This study confirmed the occurrence of lipid peroxidation in the lung during ozone exposure and revealed an enzymatic mechanism against damage. An apparent compensation mechanism is that with increased lipid peroxides there is increased activity of GSH peroxidase, which in turn increases lipid peroxide catabolism. The increased activities of GSH reductase and G-6-P dehydrogenase also function in the protective chain by providing increased levels of GSH and NADPH, respectively. Postdoctoral fellow of the American Society for Clinical Nutrition sponsored by the National Vitamin Foundation.     

Effect of dietary n−3 polyunsaturated fatty acids on cholesterol synthesis and degradation in rats of different ages

Male Sprague-Dawley rats four weeks or eight months of age were fed purified diets containing 10% fat, either as a blend of safflower oil and palm olein (polyunsaturated fatty acids, PUFA, 34%), a blend of linseed oil and palm olein (PUFA, 33%) or sardine oil (PUFA, 33%) for four weeks. In other trials, sterol contents were made equivalent by supplementing cholesterol to a blend of corn oil and palm olein (PUFA, 30%) or phytosterol to sardine oil (PUFA, 30%). Fish oil was hypolipidemic in rats of different ages, but it tended to increase liver cholesterol in adult animals and this was not improved by the addition of phytosterol. The age-dependent increase in liver cholesterol was not duplicated in rats fed a vegetable fat blend supplemented with cholesterol. At both ages, liver 3-hydroxy-3-methylglutaryl coenzyme A reductase activity was lower in the sardine oil than in the other groups. There were no significant age- or diet-related differences in the activity of liver cholesterol 7α-hydroxylase. Fecal steroid excretion was comparable in age-matched rats fed diets supplemented either with cholesterol or phystosterol. Sardine oil reduced the Δ6-desaturase activity markedly as compared with linseed oil, and age-dependent reduction of the desaturase activity was observed in all dietary groups examined. Thus, the results showed a specific effect of fish oil on lipid metabolism.     

Fatty Acid Composition,Oxidative Stability,and Radical Scavenging Activity of Vegetable Oil Blends with Coconut Oil

Coconut (Cocos nucifera) contains 55–65% oil, having C12:0 as the major fatty acid. Coconut oil has >90% saturates and is deficient in monounsaturates (6%), polyunsaturates (1%), and total tocopherols (29 mg/kg). However, coconut oil contains medium chain fatty acids (58%), which are easily absorbed into the body. Therefore, blends of coconut oil (20–80% incorporation of coconut oil) with other vegetable oils (i.e. palm, rice bran, sesame, mustard, sunflower, groundnut, safflower, and soybean) were prepared. Consequently, seven blends prepared for coconut oil consumers contained improved amounts of monounsaturates (8–36%, p < 0.03), polyunsaturates (4–35%, p < 0.03), total tocopherols (111–582 mg/kg, p < 0.02), and 5–33% (p < 0.02) of DPPH (2,2-diphenyl-1-picrylhydrazyl free radicals) scavenging activity. In addition, seven blends prepared for non-coconut oil consumers contained 11–13% of medium chain fatty acids. Coconut oil + sunflower oil and coconut oil + rice bran oil blends also exhibited 36.7–89.7% (p < 0.0005) and 66.4–80.5% (p < 0.0313) reductions in peroxide formation in comparison to the individual sunflower oil and rice bran oil, respectively. It was concluded that blending coconut oil with other vegetable oils provides medium chain fatty acids and oxidative stability to the blends, while coconut oil will be enriched with polyunsaturates, monounsaturates, natural antioxidants, and a greater radical scavenging activity.     

椰子油和大豆油的乙氧基化物对小鼠肝脏的脂质过氧化效应研究

为探讨椰子油乙氧基化物-36EO(COE-36)和大豆油乙氧基化物-42EO(SOE-42)对小鼠肝脏的脂质过氧化作用,采用腹腔注射技术,测定COE-36处理组、SOE-42处理组、氯化镉阳性对照组(小鼠单位体质量的氯化镉用量为2.5μg.g-1)和生理盐水阴性对照组小鼠肝脏超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性和丙二醛(MDA)生成量。结果表明,氯化镉显著抑制了小鼠肝脏SOD和CAT活性,增加了MDA生成量;在所测3个指标中,COE-36和SOE-42的3个用量组(以小鼠单位体质量的用药量计)与生理盐水阴性对照组相比均无显著性差异;与氯化镉阳性对照组相比,不同用量COE-36作用下SOD和CAT活性变化、不同用量SOE-42作用下CAT活性变化以及低用量(3 mg.g-1)COE-36或SOE-42作用下MDA生成量变化均有显著性差异,说明在所试用量(3～5 mg.g-1)下,这2种表面活性剂不会引起小鼠肝细胞的脂质过氧化。     

HPLC of triglycerides

Triglyceride separation was investigated on a reverse phase high performance liquid chromatography (HPLC) column using two different solvent systems. Complete separation of model compounds differing by two methylene groups was achieved. Partial or complete separation was also observed in critical pairs; for example, the different types of triglycerides consisting of palmitic and oleic acids. This observation was confirmed on natural oils (coconut oil, palm kernel oil).     

Comparative effects of α- and γ-linolenic acids on rat liver fatty acid oxidation

It has been reported that both n−3 and n−6 octadecatrienoic acids can increase hepatic fatty acid oxidation activity. It remains unclear, however, whether different enzymes in fatty acid oxidation show a similar response to n−3 and n−6 octadecatrienoic acids. The activity of hepatic fatty acid oxidation enzymes in rats fed an oil mixture rich in α-linolenic acid (18:3n−3) and borage oil rich in γ-linolenic acid (18:3n−6) was therefore compared to that in rats fed an oil mixture rich in linoleic acid (18:2n−6) and a saturated fat (palm oil) in this study. Linseed oil served as the source of 18:3n−3 for the oil mixture rich in this octadecatrienoic acid and contained 30.6% 18:3n−3 but not 18:3n−6. Borage oil contained 25.7% 18:3n−6 and 4.5% 18:3n−3. Groups of seven rats each were fed diets containing 15% various fats for 15 d. The oxidation rate of palmitoyl-CoA in the peroxisomes was higher in rats fed a fat mixture rich in 18:3n−3 (3.03 nmol/min/mg protein) and borage oil (2.89 nmol/min/mg protein) than in rats fed palm oil (2.08 nmol/min/mg protein) and a fat mixture rich in 18:2n−6 (2.15 nmol/min/mg protein). The mitochondrial palmitoyl-CoA oxidation rate was highest in rats fed a fat mixture rich in 18:3n−3 (1.93 nmol/min/mg protein), but no significant differences in this parameter were seen among the other groups (1.25–1.46 nmol/min/mg protein). Compared to palm oil and fat mixtures rich in 18:2n−6, a fat mixture rich in 18:3n−3 and borage oil significantly increased the hepatic activity of carnitine palmitoyl-transferase and acyl-CoA oxidase. Compared to palm oil and a fat mixture rich in 18:2n−6, a fat mixture rich in 18:3n−3, but not fats rich in 18:3n−6, significantly decreased 3-hydroxyacyl-CoA dehydrogenase activity. Compared to palm oil and a fat mixture rich in 18:2n−6, borage oil profoundly decreased mitochondrial acyl-CoA dehydrogenase activity, but a fat mixture rich in 18:3n−3 increased it. 2,4-Dienoyl-CoA reductase activity was significantly lower in rats fed palm oil than in other groups. Compared to other fats, borage oil significantly increased Δ³, Δ²-enoyl-CoA isomerase activity. Activity was also significantly higher in rats fed 18:2n−6 oil than in those fed palm oil. It was confirmed that both dietary 18:3n−6 and 18:3n−3 increased fatty acid oxidation activity in the liver. These two dietary octadecatrienoic acids differ considerably, however, in how they affect individual fatty acid oxidation enzymes.     

Dietary triacylglycerol structure and saturated fat alter plasma and tissue fatty acids in piglets

Human and pig milk triacylglycerols contain a large proportion of palmitic acid (16:0) which is predominately esterified in the 2-position. Other dietary fats contain variable amounts of 16:0, with unsaturated fatty acids predominantly esterified in the 2-position. These studies determined if the amount or position of 16:0 in dietary fat influences the composition or distribution of liver, adipose tissue, lung, or plasma fatty acids in developing piglets. Piglets were fed to 18 d with sow milk or formula with saturated fat from medium-chain triglyceride (MCT), coconut or palm oil, or synthesized triacylglycerols (synthesized to specifically direct 16:0 to the 2-position) with, in total fatty acids, 30.7, 4.3, 6.5, 27.0, and 29.6% 16:0, and in 2-position fatty acids, 55.3, 0.4, 1.3, 4.4, and 69.9% 16:0, respectively. The percentage of 16:0 in the 2-position of adipose fat from piglets fed sow milk, palm oil, and synthesized triacylglycerols were similar and higher than in piglets fed MCT or coconut oil. Thus, the amount, not the position, of dietary 16:0 determines piglet adipose tissue 16:0 content. The effects of the diets on the plasma and liver triacylglycerols were similar, with significantly lower 16:0 in total and 2-position fatty acids of the MCT and coconut oil groups, and significantly higher 16:0 in the plasma and liver triacylglycerol 2-position of piglets fed the synthesized triacylglycerols rather than sow milk or palm oil. The lung phospholipid total and 2-position 16:0 was significantly lower in the MCT, coconut, and palm oil groups, but similar in the synthesized triacylglycerol group and sow milk group. The lung phospholipid total and 2-position percentage of arachidonic acid (20:4n-6) was significantly lower in all of the formula-fed piglets than in milk-fed piglets. The physiological significance of this is not known.     

The Role of Oil Phase in the Stability and Physicochemical Properties of Oil-in-Water Emulsions in the Presence of Gum Tragacanth

Different emulsions based on six types of vegetable oils (sunflower, canola, sesame, olive, coconut, and palm olein) were studied to investigate the role of the oil phase in the stability and physicochemical characteristics of oil-in-water emulsions prepared with gum tragacanth. The results indicated that the stability, rheological parameters, and size distribution of emulsions were dependent on the oil type. Based on the interfacial tension value, the type of oil did not have a significant effect on the gum tragacanth-emulsifying properties. The formulation based on sunflower and coconut oil led to producing more stable emulsion and a sample containing palm olein resulted in an unstable emulsion. Rheological analysis revealed that the sample based on palm olein showed the lowest consistency coefficient (2.10 ± 0.05 Pas ⁿ), elastic modulus (3.90 ± 0.21 Pa), and energy of cohesion (80.87 ± 1.1 J m⁻³). This study revealed that using oils with lower viscosity and higher density led to the higher stability of the emulsion samples.     

Effects of feeding chenodeoxycholic acid on metabolism of cholesterol and bile acids in germ-free rats

The aim of this investigation was to study the influence of chenodeoxycholic acid administration on cholesterol and bile acid synthesis in germ-free rats. Seven rats were fed a basal diet and 2 groups of 4 rats received the same diet supplemented with 0.4 and 1% chenodeoxycholic acid, respectively. After 6 weeks, feces were collected in one 3- and one 4-day pool for analysis of cholesterol and bile acids. When the sampling period was finished, the rats were killed and the liver microsomal fractions isolated. The activities of HMG CoA reductase and cholesterol 7α-hydroxylase were determined, the 7α-hydroxylase by a mass fragmentographic method. The 2 dominating bile acids in the untreated rats were cholic acid and β-muricholic acid. During treatment with chenodeoxycholic acid, 60–70% of this bile acid was converted into α- and β-muricholic acid, indicating a high activity of the 6β-hydroxylase. The excretion of cholic acid was almost completely inhibited and the 7α-hydroxylase activity was decreased ca 75% in the rats fed 1% chenodeoxycholic acid. The activity of the hepatic HMG CoA reductase was unchanged. The fecal excretion of cholesterol increased 2–3 times. An accumulation of cholesterol was seen in the rats treated with 1% chenodeoxycholic acid, which was probably a result of the decreased catabolism of cholesterol to bile acids.