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Styrene is a volatile organic compound (VOC) that is widely used as a solvent in many industrial settings. Chronic exposure to styrene can result in irritation of the mucosa of the upper respiratory tract. Contact of styrene with epithelial cells stimulates the expression of a variety of inflammatory mediators, including the chemotactic cytokine monocyte chemoattractant protein-1 (MCP-1). To characterise the underlying mechanisms of the induction of inflammatory signals by styrene, we investigated the influence of this compound on the induction of oxidative stress and the activation of the nuclear factor-kappa B (NF-kappaB) signalling pathway in human lung epithelial cells (A549). The results demonstrate that styrene-induced MCP-1 expression, as well as the expression of the oxidative stress marker glutathione S-transferase (GST), is associated with a concentration dependent pattern of NF-kappaB activity. An inhibitor of NF-kappaB, IKK-NBD, and the anti-inflammatory antioxidant N-acetylcysteine (NAC) were both effective in suppressing styrene-induced MCP-1 secretion. In addition, NAC was capable of inhibiting the upregulation of GST expression. Our findings suggest that the activation of the NF-kappaB signalling pathway by styrene is mediated via a redox-sensitive mechanism.

Protein-associated amino acids are supposed to play a role in sterol regulatory element-binding protein (SREBP)-mediated regulation of lipid metabolism. This study investigates the effects of cysteine on expression of SREBP-regulated hepatic genes.HepG2 cells which are an accepted model for the study of the lipid metabolism were treated with L-cysteine under different conditions.Exposure of cells to L-cysteine reduced the mRNA concentrations of SREBP-1c (-35 to -43%) and its target genes fatty acid synthase (FAS; -20 to -50%), glucose-6-phosphate-dehydrogenase (G6PDH; -31 to -35%), and stearoyl-coenzyme A desaturase (SCD)1 (-34 to -50%). Cells treated with L-cysteine had 47% higher glutathione and 47% lower triglyceride concentrations than control cells. In cells which were concurrently treated with L-cysteine and L-buthionine-[S,R]-sulfoximine, an inhibitor of enzymatic glutathione synthesis, no down-regulation of the gene expression was observed. Pro-oxidant CuSO(4) up-regulated SREBP-1c (+71%), FAS (+165%), G6PDH (+84%) and SCD1 (+96%) mRNA abundance compared to control cells, but when cells were concurrently treated with L-cysteine, the gene expression remained at control level.The results show that L-cysteine rapidly down-regulates the transcription of genes involved in fatty acid biosynthesis via a mechanism that appears to be mediated by an improved glutathione status.

Peroxisome proliferator-activated receptor (PPAR)-alpha mediates an adaptive response to fasting by up-regulation of genes involved in fatty acid oxidation and ketone body synthesis. Ketone bodies are transferred in and out of cells by monocarboxylate transporter (MCT)-1. In this study we observed for the first time that activation of PPARalpha in rats by clofibrate treatment or fasting increased hepatic mRNA concentration of MCT1. In Fao rat hepatoma cells, incubation with the PPARalpha agonist WY 14,643 increased mRNA concentration of MCT1 whereas the PPARgamma agonist troglitazone did not. To elucidate whether up-regulation of MCT1 is indeed mediated by PPARalpha we treated wild-type and PPARalpha-null mice with WY 14,643. In wild-type mice, treatment with WY 14,643 increased mRNA concentrations of MCT1 in liver, kidney and small intestine whereas no up-regulation was observed in PPARalpha-null mice.

Administration of oxidized oils to rats or pigs causes a reduction of their cholesterol concentrations in liver and plasma. The reason for this effect is unknown. We tested the hypothesis that oxidized oils lower cholesterol concentrations by inhibiting the proteolytic activation of sterol regulatory element-binding protein (SREBP)-2 in the liver and transcription of its target genes involved in cholesterol synthesis and uptake through an upregulation of gene expression of insulin-induced genes (Insig). For 6 d, 18 rats were orally administered either sunflower oil (control group) or an oxidized oil prepared by heating sunflower oil. Rats administered the oxidized oil had higher messenger RNA (mRNA) concentrations of acyl-CoA oxidase and cytochrome P450 4A1 in the liver than control rats (P < 0.05), indicative of activation of PPARalpha. Furthermore, rats administered the oxidized oil had higher mRNA concentrations of Insig-1 and Insig-2a, a lower concentration of the mature SREBP-2 in the nucleus, lower mRNA concentrations of the SREBP-2 target genes 3-hydroxy-3-methylglutaryl CoA reductase and LDL receptor in their livers, and a lower concentration of cholesterol in liver, plasma, VLDL, and HDL than control rats (P < 0.05). In conclusion, this study shows that reduced cholesterol concentrations in liver and plasma of rats administered an oxidized oil were due to an inhibition of the activation of SREBP-2 by an upregulation of Insig, which in turn inhibited transcription of proteins involved in hepatic cholesterol synthesis and uptake.

It has been shown that dietary oxidized fats influence thyroid function in rats and pigs. Mechanisms underlying this phenomenon are unknown. This study was performed to investigate whether 13-hydroperoxy-9,11-octadecadienic acid (13-HPODE), a primary oxidation product of linoleic acid, affects expression of genes involved in thyroid hormone synthesis and formation of hydrogen peroxide in primary porcine thyrocytes. Thyrocytes were treated with 13-HPODE in concentrations between 20 and 100 μM. Cells treated with vehicle alone ("control cells") or with equivalent concentrations of linoleic acid were considered as controls. Treatment of cells with 13-HPODE did not affect cell viability but increased the activities of the antioxidant enzymes superoxide dismutase and glutathione peroxidase (p < 0.05) compared to control cells or cells treated with linoleic acid. Relative mRNA concentrations of genes involved in thyroid hormone synthesis like sodium iodide symporter, thyrotropin receptor, and thyroid peroxidase, as well as iodide uptake, did not differ between cells treated with 13-HPODE and control cells or cells treated with linoleic acid. Treatment of cells with 13-HPODE, however, reduced the relative mRNA concentrations of dual oxidase-2 and the formation of hydrogen peroxide compared to control cells or cells treated with linoleic acid (p < 0.05). Because the production of hydrogen peroxide is rate-limiting for the synthesis of thyroid hormones, it is suggested that 13-HPODE could have an impact on the formation of thyroid hormones in the thyroid gland.

Atherosclerosis is characterized by extensive thickening of the arterial intima partially resulting from deposition of collagen by vascular smooth muscle cells (SMCs). Polyunsaturated fatty acids stimulate collagen formation through NF-kappaB activation.The present study aimed to explore the effect of conjugated linoleic acids (CLAs) which are known to inhibit NF-kappaB activation on collagen formation by SMCs.Vascular SMCs were cultured with 50 micromol/l of CLA isomers (c9t11-CLA, t10c12-CLA) or linoleic acid (LA) and analysed for collagen formation and NF-kappaB p50 transactivation.Treatment with CLA isomers but not LA significantly reduced PDGF-stimulated [(3)H] proline incorporation into cell layer protein of SMCs without altering cell proliferation. Simultaneous treatment with the PPARgamma inhibitor T0070907 abrogated this effect. Treatment of SMCs with c9t11-CLA and t10c12-CLA significantly reduced PDGF-induced NF-kappaB p50 activation.CLA isomers inhibit PDGF-stimulated collagen production by vascular SMCs, which is considered to be a hallmark of atherosclerosis, in a PPARgamma-dependent manner. Whether inhibition of the NF-kappaB-pathway is of significance for the reduction of collagen formation by CLA isomers needs further investigation.

This study investigated the effect of clofibrate treatment on expression of target genes of peroxisome proliferator-activated receptor (PPAR)-α and various genes of the lipid metabolism in liver and adipose tissue of pigs. An experiment with 18 pigs was performed in which pigs were fed either a control diet or the same diet supplemented with 5 g clofibrate/kg for 28 days. Pigs treated with clofibrate had heavier livers, moderately increased mRNA concentrations of various PPAR-α target genes in liver and adipose tissue, a higher concentration of 3-hydroxybutyrate, and markedly lower concentrations of triglycerides and cholesterol in plasma and lipoproteins than control pigs ( P < 0.05). mRNA concentrations of sterol regulatory element-binding proteins (SREBP)-1 and -2, insulin-induced genes ( Insig) -1 and Insig-2, and the SREBP target genes acetyl-CoA carboxylase, 3-methyl-3-hydroxyglutaryl-CoA reductase, and low-density lipoprotein receptor in liver and adipose tissue and mRNA concentrations of apolipoproteins A-I, A-II, and C-III in the liver were not different between both groups of pigs. In conclusion, this study shows that clofibrate treatment activates PPAR-α in liver and adipose tissue and has a strong hypotriglyceridemic and hypocholesterolemic effect in pigs. The finding that mRNA concentrations of some proteins responsible for the hypolipidemic action of fibrates in humans were not altered suggests that there were certain differences in the mode of action compared with humans. It is also shown that PPAR-α activation by clofibrate does not affect hepatic expression of SREBP target genes involved in synthesis of triglycerides and cholesterol homeostasis in liver and adipose tissue of pigs.

Gene expression and activity of matrix-metalloproteinases (MMP)-2 and -9 in macrophages are reduced through peroxisome proliferator-activated receptor gamma (PPARgamma)-dependent inhibition of NF-kappaB. Since conjugated linoleic acids (CLAs) are PPARgamma ligands and known to inhibit NF-kappaB via PPARgamma, we studied whether CLA isomers are capable of reducing gene expression and gelatinolytic activity of MMP-2 and -9 in PMA-differentiated THP-1 macrophages, which has not yet been investigated. Incubation of PMA-differentiated THP-1 cells with either c9t11-CLA, t10c12-CLA or linoleic acid (LA), as a reference fatty acid, resulted in a significant incorporation of the respective fatty acids into total cell lipids relative to control cells (P

Conjugated linoleic acids (CLAs) are biologically active lipid compounds exerting anti-atherogenic actions in vivo without exact knowledge about the underlying mechanisms. Recently, CLAs were shown to lower the release of vasoactive prostanoids from vascular smooth muscle cells (SMCs) which play a central role in atherosclerosis. Since SMCs from different vascular locations were shown to exert differential actions in response to a common stimulus, the present study aimed to explore potential differential effects of CLA isomers on the release of the prostanoids PGE2 and PGI2 from coronary artery and aortic SMCs. For this purpose, human aortic and coronary artery SMCs were incubated with 5 and 50 μmol/L of cis-9, trans-11 CLA and trans-10, cis-12 CLA for 24 hours and analyzed for fatty acid composition and the release of prostaglandins E2 and I2 (PGE2 and PGI2). Incubations were performed in the absence (basal conditions) and in the presence of 10 ng/mL of the cytokine tumor necrosis factor-α (TNFα) (cytokine-stimulated conditions). Fatty acid analysis revealed a similar degree of incorporation of CLA isomers and dose-dependent reduction of arachidonic acid in total cell lipids of both types of vascular SMCs following treatment with CLA. The release of PGE2 and PGI2 was dose-dependently inhibited by either CLA isomer from both types of vascular SMCs. The inhibitory potential of CLA isomers on the release of prostanoids was slightly different between basal and cytokine-stimulated conditions. In conclusion, the present findings suggest that the action of CLA isomers on the release of vasoactive prostanoids from vascular SMCs is largely independent of the vascular location; e.g., coronary arteries or systemic vasculature (aorta), but partially depends on the pathophysiological status of SMCs. The observed anti-inflammatory effect of CLAs may contribute to the anti-atherogenic actions of CLA.

Background In rodents treatment with fibrates causes hepatocarcinogenesis, probably as a result of oxidative stress and an impaired balance between apoptosis and cell proliferation in the liver. There is some debate whether fibrates could also induce liver cancer in species not responsive to peroxisome proliferation. In this study the effect of clofibrate treatment on peroxisome proliferation, production of oxidative stress, gene expression of pro- and anti-apoptotic genes and proto-oncogenes was investigated in the liver of pigs, a non-proliferating species. Results Pigs treated with clofibrate had heavier livers (+16%), higher peroxisome counts (+61%), higher mRNA concentration of acyl-CoA oxidase (+66%), a higher activity of catalase (+41%) but lower concentrations of hydrogen peroxide (-32%) in the liver than control pigs (P < 0.05); concentrations of lipid peroxidation products (thiobarbituric acid-reactive substances, conjugated dienes) and total and reduced glutathione in the liver did not differ between both groups. Clofibrate treated pigs also had higher hepatic mRNA concentrations of bax and the proto-oncogenes c-myc and c-jun and a lower mRNA concentration of bcl-XL than control pigs (P < 0.05). Conclusion The data of this study show that clofibrate treatment induces moderate peroxisome proliferation but does not cause oxidative stress in the liver of pigs. Gene expression analysis indicates that clofibrate treatment did not inhibit but rather stimulated apoptosis in the liver of these animals. It is also shown that clofibrate increases the expression of the proto-oncogenes c-myc and c-jun in the liver, an event which could be critical with respect to carcinogenesis. As the extent of peroxisome proliferation by clofibrate was similar to that observed in humans, the pig can be regarded as a useful model for investigating the effects of peroxisome proliferators on liver function and hepatocarcinogenesis.

The present rat study was conducted to test whether hyper-homocysteinemia induced by dietary homocysteine (Hcy) alters the cholesterol concentration in plasma and tissue and the gene expression of genes involved in cholesterol biosynthesis and uptake. Therefore, rats were fed 100 or 200 mg Hcy per kilogram body mass per day (Hcy100 group and Hcy200 group, respectively) as dl-homocysteine thiolactone, or an Hcy-free diet, which served as control, over 14 days. Rats from the Hcy100 group and the Hcy200 group had higher plasma Hcy concentrations (34.4 +/- 4.6 and 69.4 +/- 11.5 microM, respectively) than rats fed an Hcy-free diet (9.5 +/- 1.7 microM). The concentration of Hcy in liver was 2.6 and 3.8 times higher, and in small intestine was 2.6 and 5.1 times higher, in the Hcy100 group and the Hcy200 group, respectively, than in control rats (P0.05). The concentrations of cholesterol in plasma, lipoproteins, liver, and small intestine and the relative mRNA concentrations of sterol regulatory element-binding protein 2 (SREBP-2), 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, and low-density lipoprotein (LDL) receptor in liver and small intestine were not influenced by dl-homocysteine thiolactone supplementation. In conclusion, in view of the experimental conditions used here, increased plasma and tissue concentrations of Hcy do not alter cholesterol metabolism of liver and intestine.

Nationale Differenzen haben die Geschichte Europas der letzten 150 Jahre bestimmt. Diesseits dieser Differenzen bleiben weiterhin Differenzen wirksam, die die Vorgeschichte der Nationalstaaten in Europa gepragt haben. Geographisch gesehen sind dies Nord-Sud-Differenzen und Ost-West-Differenzen, die ihrerseits mit sozialen Strukturen zu tun haben: kulturellen Differenzen, (katholische versus protestantische Raume in Europa), und okonomischen Differenzen (feudale Agrarordnungen versus stadtburgerliche Handler- und Handwerkerkulturen). Stein Rokkan hat dies als das besondere System von Spaltungsstrukturen („cleavage structure“) in Europa bezeichnet.

Alcoholic fatty liver results from an impaired fatty acid catabolism due to blockade of PPARalpha and increased lipogenesis due to activation of sterol regulatory element-binding protein (SREBP)-1c. Because both oxidized fats (OF) and conjugated linoleic acids (CLA) have been demonstrated in rats to activate hepatic PPARalpha, we tested the hypothesis that these fats are able to prevent ethanol-induced triacylglycerol accumulation in the liver by upregulation of PPARalpha-responsive genes. Forty-eight male rats were assigned to 6 groups and fed isocaloric liquid diets containing either sunflower oil (SFO) as a control fat, OF prepared by heating of SFO, or CLA, in the presence and absence of ethanol, for 4 wk. Administration of ethanol lowered mRNA concentrations of PPARalpha and the PPARalpha-responsive genes medium chain acyl-CoA dehydrogenase, long chain acyl-CoA dehydrogenase, acyl-CoA oxidase, carnitine palmitoyl-CoA transferase I, and cytochrome P450 4A1 and increased triacylglycerol concentrations in the liver (P < 0.05). OF increased hepatic mRNA concentrations of PPARalpha-responsive genes and lowered hepatic triacylglycerol concentrations compared with SFO (P < 0.05) whereas CLA did not. Rats fed OF with ethanol had similar mRNA concentrations of PPARalpha-responsive genes and similar triacylglycerol concentrations in the liver as rats fed SFO or CLA without ethanol. In contrast, hepatic mRNA concentrations of SREBP-1c and fatty acid synthase were not altered by OF or CLA compared with SFO. This study shows that OF prevents an alcohol-induced triacylglycerol accumulation in rats possibly by upregulation of hepatic PPARalpha-responsive genes involved in oxidation of fatty acids, whereas CLA does not exert such an effect.

Previous studies have shown that supplementation of sow diets with L-carnitine increases the body weight of piglets at birth. This study was conducted to elucidate the reasons for this phenomenon. Three experiments with 24 (experiment 1), 40 (experiment 2) and 12 (experiment 3) sows were conducted. In all three experiments, sows were allotted to two groups which had free access to a nutritionally adequate diet. Sows of one group were supplemented with 125 mg L-carnitine/day during pregnancy; sows of the other group (control group) did not receive L-carnitine. In experiment 1, plasma samples were collected at day 95 of pregnancy, in experiment 2 plasma samples were collected at days 80 and 100 of pregnancy. In experiment 3, chorions of the sows were collected at parturition. L-carnitine-treated sows had higher plasma concentrations of total L-carnitine than control sows (p < 0.05). The number of piglets born and weights of litter and individual piglets at birth were not different between both groups in all three experiments. L-carnitine-treated sows had higher plasma concentrations of insulin-like growth factor-I (IGF-I) on day 80 of pregnancy (experiment 2, p < 0.05) and on day 95 (experiment 1, p < 0.10), and a higher plasma concentration of IGF-II on day 80 (experiment 2, p < 0.05) than control sows. Moreover, sows supplemented with L-carnitine had heavier chorions (+22%, p =0.10) with greater amounts of protein (+45%, p < 0.05) and DNA (+38%, p < 0.10) and a higher protein concentration of glucose transporter-1 (+62%, p < 0.05). Plasma concentrations of 17beta-oestradiol, progesterone and thyroid hormones as well as concentrations of urea and total free amino acids were not different between both groups of sows. Plasma concentrations of non-esterified fatty acids, ketone bodies, triacylglycerols and cholesterol were also largely indifferent between both groups of sows. In conclusion, this study shows that L-carnitine has less influence on lipid metabolism and utilization of nitrogen in pregnant sows but increases their plasma concentrations of IGFs. This in turn may enhance development of the placentae and the intrauterine nutrition of the fetuses. This may be the reason for increased birth weights observed in recent studies in sows supplemented with L-carnitine.

It is known that various dietary plant proteins are capable of influencing the lipid metabolism of human subjects and animals when compared with casein. Less, however, is known about the effects of fish protein on the cholesterol and triacylglycerol metabolism. Therefore, two experiments were conducted in which rats were fed diets containing 200 g of either fish protein, prepared from Alaska pollack fillets, or casein, which served as control, per kilogram, over 20 and 22 d, respectively. As parameters of lipid metabolism, the concentrations of cholesterol and triacylglycerols in the plasma and liver, the faecal excretion of bile acids and the hepatic expression of genes encoding proteins involved in lipid homeostasis were determined. In both experiments, rats fed fish protein had higher concentrations of cholesteryl esters in the liver, a lower concentration of cholesterol in the HDL fraction (rho1.063 kg/l) and lower plasma triacylglycerol concentrations than rats fed casein (P0.05). The gene expression analysis performed in experiment 2 showed that rats fed fish protein had higher relative mRNA concentrations of sterol regulatory element-binding protein (SREBP)-2, 3-hydroxy-3-methylglutaryl coenzyme A reductase, LDL receptor, apo AI, scavenger receptor B1 and lecithin-cholesterol-acyltransferase in their liver than did rats fed casein (P0.05). The faecal excretion of bile acids and the mRNA concentrations of cholesterol 7alpha-hydroxylase, SREBP-1c and corresponding target genes were not altered. These findings show that fish protein had multiple effects on plasma and liver lipids that were at least in part caused by an altered expression of the hepatic genes involved in lipid homeostasis.

It has been shown that l-carnitine supplementation of sows increases their milk production and the postnatal growth of the suckling piglets. To test the hypothesis that this effect is due to an improved suckling behaviour of the piglets, two experiments with sows were performed. Two groups of thirteen or ten sows each (in experiments 1 and 2, respectively) were fed diets with or without supplemental l-carnitine during pregnancy (125mg/d) and lactation (250mg/d). After birth, the litters of all sows were standardised to equal sizes of eleven and nine piglets per litter in experiments 1 and 2, respectively. In experiment 1, the piglets of l-carnitine-supplemented sows had a higher total suckling time per day on days 3, 6 and 9, and greater weight gains during the suckling period, than the piglets of control sows (PP

This study was conducted to investigate the effects of rumen-protected tryptophan (125 g tryptophan per day) in heifers and dairy cows. Blood samples from dairy cows and heifers were collected for 24h in 3-h intervals on the day before tryptophan supplementation, on day 2, 5 and 7 of tryptophan supplementation, and in heifers additionally on d 14 after tryptophan supplementation was ceased. Plasma tryptophan, melatonin, serotonin, and prolactin concentrations were determined. Tryptophan plasma concentrations on d 5 were augmented at day (11:00 h) and nighttime (02:00 h), (P0.05) in response to tryptophan supplementation in heifers by 119% and in dairy cows by 47%, respectively, as compared with d 0. Melatonin increased (P0.05) in response to tryptophan supplementation in heifers, but not in cows. The effect of tryptophan supplementation on plasma tryptophan and melatonin was reversible as demonstrated in heifers on d 14 after cessation of tryptophan supplementation. Serotonin and prolactin in plasma did not respond to tryptophan supplementation. However, milk yield during morning milking increased significantly in tryptophan supplemented cows on d 1, 3 and 4 as compared to the day before tryptophan supplementation. Additional blood samples were taken during afternoon milking in cows at 1-min intervals for the analyses of oxytocin and prolactin on the day before the start and on d 7 of tryptophan supplementation. Milk flow curves were recorded during milking. No effect of tryptophan supplementation on the milking related release of oxytocin and prolactin and on any characteristic of milk flow was observed. In conclusion, tryptophan supplementation caused increased plasma tryptophan in cows and heifers and plasma melatonin in heifers. However, plasma serotonin, prolactin and oxytocin release in cows remained unchanged by tryptophan supplementation. Milk yield at morning milking increased slightly and transiently in response to tryptophan supplementation.

In this study, the proportions of conjugated linoleic acids (CLA) in total lipids of plasma, lipoproteins and erythrocytes from maternal blood and from venous cord blood of 20 pregnant women consuming conventional western diets after delivery were determined. cis-9, trans-11 CLA was the only isomer detected, and its proportions in maternal blood lipids were relatively low. Mean proportions in plasma, lipoproteins and erythrocytes of mothers were between 0.20 and 0.25 mol/100 mol of total fatty acids. Proportions in cord blood lipids were even lower than those of maternal lipids (values in mol/100 mol: plasma, 0.19+/-0.04; VLDL, 0.20+/-0.06; LDL, 0.15+/-0.03; HDL, 0.14+/-0.06; erythrocytes, 0.12+/-0.05). There was some significant (P

Recently, it has been shown that supplementation of sows with L-carnitine increases their plasma concentrations of insulin-like growth factor (IGF)-I, and it has been hypothesized that this may stimulate fetal myogenesis. This study was performed to investigate whether piglets of sows supplemented with L-carnitine differ in muscle fibre characteristics, chemical body composition and postnatal growth capability from pigs of control sows. Muscle fibre characteristics and chemical body composition were determined at weaning in 21 piglets of control sows and 21 piglets of sows treated with L-carnitine with similar body weights; postnatal growth capability was determined from weaning until slaughter at a body weight of 118 kg in 80 pigs of control sows and 80 pigs of sows treated with L-camitine which had also similar body weights at weaning. Piglets of sows supplemented with L-carnitine did not differ in number, area, diameter and type (percentages of slow twitch oxidative + fast twitch oxidative fibres, and fast twitch glycolytic fibres) of muscle fibres in m. longissimus dorsi and m. semitendinosus and in chermical body composition (concentrations of dry matter, crude protein, crude fat) from piglets of control sows. Postnatal growth capability (body weight gains, feed conversion ratio) from weaning to slaughter as well as carcass composition (carcass yield, meat thickness, fat thickness) was also not different between pigs of sows treated with L-carnitine and pigs of control sows. In conclusion, data of this study do not support the hypothesis that L-carnitine supplementation of sows during pregnancy enhances fetal muscle fibre development and increases postnatal growth capability of the offspring.

Methionine has been shown to increase plasma cholesterol in animals. In the present study, mechanisms were investigated by which methionine could alter cholesterol metabolism. In the first experiment, forty growing rats were fed four casein-based diets differing in methionine content (2·6, 3·5, 4·5 or 6·0 g/kg) for 14 d. In the second experiment, isolated rat hepatocytes were incubated in media supplemented with 50, 100 or 200 μmol/l methionine. Dietary methionine tended to increase plasma homocysteine concentrations in the rats (P=0·058). A weak positive correlation between circulating homocysteine and plasma cholesterol was observed (R20·27, P. 1·063, and in liver than rats fed 2·6 g/kg methionine. Rats fed 6 g/kg methionine had a higher hepatic expression of 3-hydroxy-3-methylglutaryl coenzyme A reductase and cholesterol-7α-hydroxylase than rats fed less methionine. The phosphatidylcholine:phosphatidylethanolamine ratio in rat liver increased with rising dietary methionine concentration; the relative mRNA concentrations of phosphatidylethanolamine N-methyltransferase and cystathionine β-synthase remained unaffected. Hepatocytes incubated in media supplemented with 100 or 200 μmol/l methionine had a higher cholesterol synthesis than hepatocytes incubated in a medium supplemented with 50μmol/l methionine; the LDL uptake in hepatocytes was independent of the methionine concentration of the medium. In conclusion, the present study suggests that dietary methionine induces hypercholesterolaemia at least in part via an enhanced hepatic cholesterol synthesis.

In this study, 13 different eluent systems containing n-hexane, n-heptane and iso-octane as main solvents and ACN, propionitrile (PCN) and butyronitrile (BCN) in concentrations between 0.1 and 0.2% as modifiers were tested for their influence on retention time shifts (RTS) and resolution of conjugated linoleic acid (CLA) methyl esters using two ChromSpher 5 Lipids columns (250 mm x 4.6 mm, 5 microm) in series. The eluent system n-hexane/PCN 0.2% showed the highest stability with an obtained RTS of 0.26 min for the cis/trans-group after 14 consecutive injections of a CLA isomer mix compared to the reference system of n-hexane/ACN 0.15% (RTS of 2.35 min). This enhanced stability is due to better solubility of PCN in n-hexane compared to ACN. The enhanced stability coincided with a negligible loss in resolution for the cis,trans/trans,cis- and the cis,cis-groups. As shown for the analysis of human aortic endothelial cells spiked with t10c12-CLA, data from CLA-analysis by Ag+-HPLC-DAD must be judged very carefully, especially at low concentrations, as coeluting matrix compounds may give false-positive results. Therefore, results should be confirmed by GC-FID and GC-MS.

In rats, oxidized fats activate the peroxisome proliferator-activated receptor alpha (PPARalpha), leading to reduced triglyceride concentrations in liver, plasma and very low density lipoproteins. Oxidation products of linoleic acid constitute an important portion of oxidized dietary fats. This study was conducted to check whether the primary lipid peroxidation product of linoleic acid, 13-hydroperoxy-9,11-octadecadienoic acid (13-HPODE), might be involved in the PPARalpha-activating effect of oxidized fats. Therefore, we examined the effect of 13-HPODE on the expression of PPARalpha target genes in the rat Fao and the human HepG2 hepatoma cell lines. In Fao cells, 13-HPODE increased the mRNA concentration of the PPARalpha target genes acyl-CoA oxidase (ACO), cytochrome P450 4A1 and carnitine-palmitoyltransferase 1A (CPT1A). Furthermore, the concentration of cellular and secreted triglycerides was reduced in Fao cells treated with 13-HPODE. Because PPARalpha mRNA was not influenced, we conclude that these effects are due to an activation of PPARalpha by 13-HPODE. In contrast, HepG2 cells seemed to be resistant to PPARalpha activation by 13-HPODE because no remarkable induction of the PPARalpha target genes ACO, CPT1A, mitochondrial HMG-CoA synthase and delta9-desaturase was observed. Consequently, cellular and secreted triglyceride levels were not changed after incubation of HepG2 cells with 13-HPODE. In conclusion, this study shows that 13-HPODE activates PPARalpha in rat Fao but not in human HepG2 hepatoma cells.

The present study investigated the effect of l-carnitine supplementation during pregnancy (125 mg/d) and lactation (250 mg/d) on milk production, litter gains and back-fat thickness in sows fed a low-energy and low-protein diet during lactation. Sows supplemented with l-carnitine produced more milk on days 11 and 18 of lactation (+18 %;PPP

Cholesterol oxidation products (COPs) can be formed in the body or in animal foods from cholesterol during food processing. A new method for the extraction and quantification of cholesterol, 7-ketocholesterol, cholestane-3beta-5alpha-6beta-triol, 25-hydroxycholesterol, 5,6alpha-epoxycholesterol, and 7beta-hydroxycholesterol by means of reversed-phase LC/atmospheric pressure chemical ionization mass spectrometry is presented. A baseline separation of all COPs was achieved, allowing a separate quantification also for isobaric compounds. The limits of detection were 15-30 ng/mL, quantification was performed from 100 ng/mL to 10 microg/mL with RSD < 2%. The method was applied successfully to the determination of cholesterol and COPs in processed foods such as pork, beef, chicken, and egg.

The objective of this study was to determine the effects of cis-9, trans-11 and trans-10, cis-12 CLA on the delta4-desaturation process in HepG2 cells. Experiments were conducted in which HepG2 cells were incubated with 25 micromol/L of those fatty acids and the concentrations of (n-6) and (n-3) polyunsaturated fatty acids in phosphatidyl choline and phosphatidyl ethanolamine were determined. In the presence of eicosapentaenoic acid, cells treated with trans-10, cis-12 CLA had a lower ratio of docosahexaenoic acid [22:6 (n-3)], the product of delta4-desaturation, to docosapentaenoic acid [22:5 (n-3)], the substrate of delta4-desaturation in both phospholipids, than control cells or cells treated with cis-9, trans-11 CLA (p < 0.05). This suggests that trans-10, cis-12 CLA suppresses the delta4-desaturation process in HepG2 cells.

The aim of this study was to find out whether concentrations of oxysterols in pig meat are affected by dietary polyunsaturated fatty acids and vitamin E. 48 growth-finishing pigs were fed diets with either palm oil or soybean oil and vitamin E concentrations of 15, 40 or 200 mg/kg. Concentrations of oxysterols were analyzed in fresh and heat-processed (180 °C, 20 min) meat (M. longissimus dorsi) and in boiled sausage prepared from meat and back fat of the animals. Concentrations of oxysterols in fresh muscle were below 5 nmol/g dry matter; they were independent of the dietary fat type and vitamin E concentration. Heating caused a large increase of oxysterol concentration (up to 55 nmol/g dry matter). This effect was reduced by increasing dietary vitamin E concentration but was independent of the dietary fat. Sausage from pigs fed soybean oil had higher concentrations of oxysterols than sausage from pigs fed palm oil; vitamin E reduced concentrations of oxysterols in sausage from pigs fed soybean oil, but not in sausage from pigs fed palm oil.

It was shown that dietary thermoxidized oils suppress gene expression of lipogenic enzymes in the liver. This study was performed to investigate whether oxidized oils also influence the activities of lipogenic enzymes in the mammary gland of lactating rats. Female rats (n = 24) were divided into two groups at 4 wk of age. They were fed for 14 wk diets with either fresh oil (a mixture of sunflower oil, linseed oil, and palm oil, 73:15:12) or oxidized oil (a mixture of sunflower oil and linseed oil, 80:20) prepared by heating at a temperature of 50 degrees C for 16 d. At the age of 12 wk, the rats were mated. At birth, litters were adjusted to 7 pups/dam. Milk was sampled at d 14 of lactation; mammary glands were taken at d 19 of lactation. Rats fed the oxidized oil had a lower activity of glucose-6-phosphate dehydrogenase (G6PDH) in their mammary glands than those fed the fresh oil (P < 0.05); the activities of fatty acid synthase (FAS) and acetyl-CoA-carboxylase in mammary glands did not differ. Relative mRNA concentrations of G6PDH, FAS, and sterol-regulatory element binding protein-1, a regulator of lipogenesis, in the mammary gland did not differ between groups. The concentrations in the milk of medium-chain fatty acids (C8-C14), the major products of fatty acid synthesis in mammary glands, also did not differ. The concentrations of triglycerides and long-chain fatty acids (C18-C22), however, were lower in the milk of rats fed the oxidized oil than in the milk of rats fed the fresh oil (P < 0.05). In conclusion, this study shows that feeding oxidized oils to lactating rats does not affect lipogenic enzymes in mammary glands but reduces the triglyceride concentrations in their milk.

Recent studies showed that piglets of sows fed diets supplemented with L-carnitine grow faster during the suckling period than piglets of control sows fed diets without L-carnitine. This study was undertaken to investigate the effect of L-carnitine supplementation in sows on milk production and milk constituents. An experiment was performed in which two groups of 20 gilts each were fed diets with or without supplemental L-carnitine during pregnancy (0 vs. 125 mg L-carnitine daily/sow) and lactation (0 vs. 250 mg L-carnitine daily/sow). The experiment was continued over two reproductive cycles. L-carnitine-treated sows had larger litters (P

The objective of this study was to determine the effects of cis-9, trans-11 and trans-10, cis-12 CLA on the release of vasoactive eicosanoids and nitric oxide (NO) in human aortic endothelial cells. Experiments were conducted in which cells were incubated with these fatty acids, and the concentrations of various eicosanoids [6-keto prostaglandin (PG) F(1alpha) as a stable product of PGI(2), thromboxane (TX) B(2) as a stable product of TXA(2), and PGE(2)] and NO in the medium were determined. Cells treated with 50 micro mol/L of either cis-9, trans-11 or trans-10, cis-12 CLA released less of all of the eicosanoids and NO than control cells treated with medium alone (P < 0.05). The ratio between the amounts of 6-keto-PGF(1alpha) and that of TXB(2) released did not differ between control cells and cells treated with either CLA isomer. Moreover, cells treated with 50 micro mol/L of cis-9, trans-11 or trans-10, cis-12 CLA had a lower amount of arachidonic acid in their phosphatidylethanolamine fraction and a lower mRNA concentration and activity of secretory phospholipase A(2) than control cells (P < 0.05). These data suggest that eicosanoid formation was impaired by a reduced availability of arachidonic acid for the cyclooxygenase pathway. In conclusion, this study shows that cis-9, trans 11-CLA and trans-10, cis-12 CLA influence the release of various eicosanoids and NO from human aortic endothelial cells. The effects observed in this study might be important because eicosanoids and NO released from endothelial cells are involved in the regulation of vessel tone and platelet aggregation. The results of the present study suggest that both CLA isomers had unfavorable effects on endothelial function.

The aim of this study was to investigate the effect of dietary oxidized fats on the lipoprotein profile and the atherogenicity of LDL. Two experiments with male Sprague-Dawley rats were conducted. In Experiment 1, diets with either fresh fat or oxidized fat, prepared by heating at temperatures of 50, 105 or 190 degrees C, containing either 25 or 250 mg alpha-tocopherol equivalents/kg were used. In Experiment 2, diets with fresh or oxidized fat, heated at a temperature of 55 degrees C, containing 25 mg alpha-tocopherol equivalents/kg, were used. In Experiment 1, rats fed all types of oxidized fats had higher concentrations of HDL cholesterol and lower ratios between plasma and HDL cholesterol than rats fed the diet containing the fresh fat. As determined from the lag time, the susceptibility of LDL to copper-induced lipid peroxidation was higher in rats fed oxidized fats heated at 105 or 190 degrees C than in rats fed the diets containing the fresh fat or the oxidized fat treated at 50 degrees C, irrespective of the dietary vitamin E concentration. However, in Experiment 2, the composition of LDL apolipoproteins and uptake of LDL by macrophages were not different between rats fed the fresh fat diet and those fed the oxidized fat diet. We conclude that ingestion of oxidized fats does not adversely affect the lipoprotein profile in the rat model used, and does not cause modifications of apolipoproteins that would lead to enhanced uptake of LDL via macrophage scavenger receptors.

The effects of dietary conjugated linoleic acid (CLA) and an alpha-glucosidase inhibitor--Bay g 5421--on tissue lipid concentrations and fatty acid composition were investigated in male broiler chicks fed a low-protein diet. The trial comprised six isoenergetic broiler diets. One diet (high-protein diet) was used as a control diet and contained 230 g crude protein per kilogram. The other five diets were low-protein diets (180 g crude protein/kg) without additional supplement, or supplemented with 20 or 40 g/kg of a CLA-enriched oil, or supplemented with 50 or 100 mg of Bay g 5421/kg. Broilers fed the low-protein diets had higher concentrations of triglycerides and cholesterol in the liver than broilers fed the high-protein diet. Broilers fed low-protein diets supplemented with CLA had a higher cholesterol concentration in plasma, lower hepatic triglyceride concentrations, higher relative concentrations of saturated fatty acids (SFA), and lower relative concentrations of monounsaturated fatty acids (MUFA) in lipids of liver, thigh muscle, and adipose than broilers fed low-protein diets without CLA supplement. Broilers fed the low-protein diets supplemented with Bay g 5421 had lower concentrations of triglycerides and cholesterol in the liver and lower concentrations of triglycerides in plasma than broilers fed the low-protein diet without supplementation. Moreover, broilers fed diets with Bay g 5421 had higher relative concentrations of polyunsaturated fatty acids and lower relative concentrations of MUFA in lipids of liver, muscle, and adipose tissue. The results show that supplementation of the low-protein diets with CLA and Bay g 5421 affected tissue lipid concentrations and fatty acid composition in broilers, which are of practical relevance with regards to meat quality.

The aim of this study was to compare the effects of dietary oxidized cholesterol and pure cholesterol on plasma and very low density lipoprotein (VLDL) lipids and on some parameters of VLDL assembly and secretion in rats fed two different dietary fats. Four groups of male growing Sprague-Dawley rats were fed diets containing pure or oxidized cholesterol (5 g/kg diet) with either coconut oil or salmon oil as dietary fat (100 g/kg diet) for 35 days. Rats fed oxidized cholesterol supplemented diets had significantly lower concentrations of triglycerides and cholesterol in plasma and VLDL than rats fed pure cholesterol supplemented diets irrespective of the type of fat. In addition, rats fed oxidized cholesterol supplemented diets had significantly lower relative concentrations of microsomal triglyceride transfer protein messenger ribonucleic acid (mRNA) than rats fed pure cholesterol supplemented diets. In contrast, hepatic lipid concentrations and the relative concentration of apolipoprotein B mRNA were not influenced by the dietary factors investigated. Parameters of hepatic lipogenesis (relative mRNA concentration of sterol regulatory element binding protein-1c and activity of glucose-6-phosphat dehydrogenase) were significantly reduced by feeding fish oil compared to coconut oil, but were not affected by the type of cholesterol. In conclusion, the data of this study suggest, that dietary oxidized cholesterol affects VLDL assembly and/or secretion by reducing the synthesis of MTP but not by impairing hepatic lipogenesis or synthesis of apolipoprotein B.

stellen die Institutionen dar, die in modernen Gesellschaften im Mittelpunkt der privaten Lebensfuhrung stehen und zur Regelung der Sexual-, Lebens- und Solidarbeziehung der jeweiligen erwachsenen Partner dienen. Hierbei finden sich historisch und kulturell grose Variationen, sowohl hinsichtlich der Partnerschaftsformen (Polygynie, Polyandrie) als auch bezuglich der konkreten Ausgestaltung der jeweiligen partnerschaftlichen Lebensform.

Offentlichkeit ist jener Freiraum zwischen Staat und Gesellschaft, in dem Institutionen thematisiert werden. Er ist weder eine politische Institution noch eine soziale Institution, sondern eine (ihrerseits institutionalisierbare) Beobachtungsinstanz und Thematisierungsinstanz politischer und sozialer Institutionen. Offentlichkeit ist ein Drittes zwischen Staat und Gesellschaft (Somers 1998), ein ausdifferenzierter Bereich politischer Kommunikation, in dem sich Sprecher an ein Publikum wenden, sowie Medien, die dieses Sprechen horbar machen. Offentlichkeit umfasst also ein soziales Feld, in dem Kommunikation mit einer gewissen Wahrscheinlichkeit stattfindet, sowie gemeinsam geteilte Relevanzstrukturen, die verstandlich machen, was kommuniziert wird (Gerhards/Neidhardt 1991; Neidhardt 1994).

Die zentralen Werke der Ungleichheitsforschung werden gut verstandlich und kompakt in ihren Hauptaussagen dargestellt.

This study was conducted to determine the interaction between the type of dietary fat (coconut oil or salmon oil) and the vitamin E concentration of the diet [10, 20, 40 or 240 mg alpha-tocopherol equivalents (alpha-toc)/kg] in relation to the concentration of 7beta-hydroxycholesterol (7beta-OH) in liver, plasma, LDL and erythrocytes of rats. In the rats whose diet contained salmon oil, the concentration of 7beta-OH was dependent on the dietary vitamin E concentration. Rats whose diet contained 10 mg alpha-toc/kg had significantly higher concentrations of 7beta-OH in all samples studied than those whose diet contained 20, 40 or 240 mg alpha-toc/kg. Increasing the dietary vitamin E concentration from 40 to 240 mg alpha-toc/kg did not reduce the concentration of 7beta-OH in any samples. In the rats whose diet contained coconut oil, the concentration of 7beta-OH was independent of the dietary vitamin E concentration in all samples. The study shows that insufficient vitamin E in the diet increases the formation of 7beta-OH in rats fed salmon oil, whereas a dietary vitamin E supply in excess of the requirement does not lower 7beta-OH concentrations compared with an adequate vitamin E supply.

Background/Aim: Recent studies demonstrated that feeding oxidized fats increases the concentrations of total and free thyroxine in blood of rats and pigs. This finding suggested that oxidized fats affect the function of the thyroid gland. This study investigates the effects of a thermally oxidized dietary fat on the morphology of the thyroid gland and on the expression of proteins (Na+/I– symporter, thyroid peroxidase) involved in the synthesis of thyroid hormones in rats at different dietary iodine concentrations. Methods: An experiment was conducted with 48 growing male Sprague-Dawley rats which were allotted to four groups of 12 animals each. According to a bifactorial experimental design, the rats received semisynthetic diets with 10% of either a fresh or an oxidized fat, with low (50 µg/kg) or adequate (400 µg/kg) iodine concentrations, over a period of 38 days. The oxidized fat was prepared by heating sunflower oil at a temperature of 55°C for a period of 5 weeks. The oxidized fat had much higher concentrations of lipid peroxidation products than the fresh fat as assessed by determining the peroxide concentrations (877 vs. 33 mEq O2/kg) and those of thiobarbituric acid reactive substances (25 vs. 0.7 µmol/kg). Results: Rats fed the diets containing oxidized fat had higher concentrations of total and free thyroxine in plasma, a greater height of thyroid epithelial cells, a smaller diameter of thyroid follicle lumen, a lower Na+/I– symporter mRNA concentration, and a higher thyroid peroxidase mRNA concentration than rats fed the fresh fat (p < 0.05 for all effects). The concentrations of triiodothyronine and thyrotropin were not different between rats fed the fresh fat and those fed the oxidized fat. The dietary iodine supply also had significant effects on some of the parameters analyzed. There were no interactions between type of fat and dietary iodine concentrations. Conclusion: The rat model used here shows that dietary oxidized fats affect the morphology and the function of the thyroid gland, irrespective of the dietary iodine supply.

Several studies have been published in recent years which suggest that L-carnitine supplementation can influence the lipid metabolism in some species and can also affect body composition of growing animals. Only few results are available so far on the effect of L-carnitine supplementation on weight reduction and body composition of animals fed an energy-deficient diet. The aim of this study was therefore to investigate whether L-carnitine supplementation combined with an energy-deficient diet can influence weight development and body composition.An experiment was conducted with 36 rats with an initial body weight of about 460 g. One-third of the rats were killed, the remainder were divided into two groups (control group, treated group) and fed a semi synthetic diet at an energy level of about half of the rats' maintenance requirement. The basal diet was essentially carnitine-free. The diet of the treated group was supplemented with L-carnitine (5 g/kg). The feeding period extended over 23 days. Experimental parameters were weight loss, composition of carcass and weights of the fat pads surrounding the kidneys, intestine and testes; several clinico-chemical plasma parameters were also determined.As was to be expected, the rats lost a considerable amount of weight on the energy-reduced diet. At the same time a shift occurred in the ratio of fat to protein in favour of protein in the carcass, leading to a marked reduction of body fat levels and a slight reduction of protein levels. There were, however, no significant differences between the control group and the treated group (with L-carnitine supplementation) with regard to any of these parameters. The clinico-chemical parameters measured in plasma (glucose, triglycerides, total cholesterol, free fatty acids, 3-hydroxybutyric acid) also showed no differences between the groups.The rat model used here did not show a positive effect of L-carnitine supplementation on weight loss and body composition of rats fed an energy-deficient diet. The animals' endogenous carnitine synthesis was obviously adequate to ensure efficient beta-oxidation of fatty acids during the catabolic phase.

The aim of this study was to investigate the effect of high dietary iron concentrations on the antioxidant status of rats fed two different types of fat. Four groups of male adult Sprague-Dawley rats were fed diets with adequate (50 mg iron supplemented per kg diet) or high (500 mg iron supplemented per kg diet) iron concentrations with either lard or salmon oil as dietary fat at 100 g/kg for 12 wk. The antioxidant status of the rats was profoundly influenced by the type of fat. Rats fed salmon oil diets had higher concentrations of thiobarbituric acid-reactive substances (TBARS) (P < 0.001), various cholesterol oxidation products (COP) (P < 0.001), total and oxidized glutathione (P < 0.05) and a lower concentration of alpha-tocopherol (P < 0.05) in liver and plasma than rats fed lard diets. The iron concentration of the diet did not influence the concentrations of TBARS, the activities of superoxide dismutase and glutathione peroxidase or the concentration of alpha-tocopherol in plasma or liver. The activity of catalase (P < 0.01) and the concentrations of total, oxidized and reduced glutathione (P < 0.05) in liver were slightly but significantly higher in rats fed high iron diets than in rats fed adequate iron diets, irrespective of the dietary fat. Rats fed the high iron diets with salmon oil, moreover, had higher concentrations of various COP in the liver (P < 0.001) than rats fed adequate iron diets with salmon oil. These results suggest that feeding a high iron diet does not generally affect the antioxidant status of rats but enhances the formation of COP, particularly if the diet is rich in polyunsaturated fatty acids.