Two different studies were conducted to reduce the overall amount of omega-6 fatty acids in broiler chickens. The first experiment was performed to determine the effects of dietary conjugated linoleic acid (CLA) and omega-3 fatty acid combination on the omega-6 fatty acid accumulation in broiler chicken breast and thigh meat. Eight broilers from each treatment were processed at 4 and 6 weeks of age, respectively. Regarding the diets containing five different fat sources, broiler chickens fed CLA and fish oil diet had a lower C20:4 (arachidonic acid, AA, n-6) deposition but showed a higher n-3/n-6 ratio in breast and thigh meat than those fed a flaxseed oil diet and CLA and flaxseed oil diet (P < 0.05). The C20:4 and n-3/n-6 ratio of breast and thigh samples from fish oil diet was similar to those of the conjugated linoleic acid and fish oil combination diet (P > 0.05). However, the addition of CLA and fish oil to the diet resulted in a increase of polyunsaturated fatty acid (PUFA) concentration in broiler chicken breast and thigh meat when compared to that of fish oil diet (P<0.05). The second experiment was conducted based on six different combination of n-3 and n-9 fatty acids. One bird per pen was processed, and each bird was weighed, and blood, liver, breast and thigh samples from the bird were collected. Although the generation of prostaglandin E2 (PGE2) was not affected due to combination of n-3 and n-9 fatty acids in our diets, the deposition of n-6 fatty acids including C18:2 and C20:4 was decreased in broiler chicken breast and/or thigh muscles as n-3 fatty acids were supplied to broiler chickens for 9 weeks. Eicosapentaenoic acid (C20:5, EPA, n-3) addition to poultry diet (FEO) did not reduce the deposition of C18:2 and/or C20:4 as much as C22:6 (FDO) did. When C20:5 and C22:6 were blended to poultry diet (FHO) and fed to broiler chickens for 9 weeks, synergistic effects were observed. Reduction of C20:4 was obtained when FHO diet was fed to broiler chickens, and it may be induced due to decreased expression of delta-6 desaturase mRNA.

We hypothesized that supplementation of dietary conjugated linoleic acid (CLA) and arginine singly or in combination would increase animal performance and meat quality by decreasing adiposity and increasing lean mass in growing-finishing pigs. Sixteen pigs (80 kg) were assigned to four treatments in a 2 x 2 factorial design, differing in dietary fatty acid and amino acid composition [control: 2.05% alanine (isonitrogenous control) plus 1% canola oil (lipid control); CLA: 2.05% alanine + 1% CLA; arginine: 1% arginine + 1% canola oil; arginine + CLA: 1% arginine + 1 CLA]. Preliminary tests indicated that up to 2% arginine was acceptable without interfering with lysine absorption. Pigs were allowed to feed free choice until reaching 110 kg. There were no significant differences across treatments in feed intake, weight gain, or feed efficiency. CLA tended to decrease carcass length (P = 0.06), whereas backfat thickness tended to be greater in pigs supplemented with arginine (P = 0.08). Arginine decreased muscle pH at 45 min postmortem (P = 0.001) and tended to increase lightness of muscle at 24 h postmortem (P = 0.07). CLA supplementation increased the concentrations of trans-isomers of 18:1 (P = 0.001) and SFA (P = 0.01) in s.c. and r.p. adipose tissue. CLA supplementation increased palmitate incorporation into total lipids in longissimus muscle (P = 0.01). Glucose oxidation to CO₂ in r.p. and s.c. adipose tissue were greater in pigs supplemented with CLA in the absence or presence of arginine (P = 0.03 and P = 0.04, respectively). The volume of s.c. adipocytes in s.c. and r.p. adipose tissues was greater in pigs supplemented with CLA, arginine, or CLA plus arginine than in control pigs (P = 0.001). Neither CLA nor arginine affected the expression of PGC-1[alpha],AMPK, mTOR, CPT-1A, FAS, or SCD (P > 0.05) in any tissues. We conclude that there was no significant interaction between arginine and CLA. Supplementary CLA or arginine to finishing-growing pigs did not modulate growth performance and did not reduce adiposity. CLA increased intramuscular fat content without deteriorating meat quality traits and increased saturated fatty acids and substrate oxidation in adipose tissues. In the presence of 1% of canola oil or CLA in the diet, arginine has the potential to deteriorate meat quality by reducing early postmortem pH and by increasing carcass fatness.

A study was performed to investigate the effect of diet modifications on skin and hair coat condition in canines. The study included 24 normal adult dogs fed a baseline diet (Ol'Roy[trademark]), during an acclimation period of 12 wk (Phase I). Nine female Beagles and 15 male Hound mix-breed dogs were used. For the next 12 wk (Phase II) the dogs were divided into three groups and fed one of three specially formulated diets. They contained similar ingredients and had similar nutrient profiles except for the following differences: Diet A contained lower but adequate amounts of dietary zinc and linoleic acid than diet B. Diet C was similar to B with respect to zinc and linoleic acid but contained more α-linolenic acid. An evaluation panel conducted skin and hair coat condition scoring on wk 0, 4, 7, and 12 (Phase I) and wk 14, 16, 19, and 24 (Phase II). The panel evaluated the dogs for glossiness, softness, scale, greasiness, and overall condition. Transepidermal water loss (TEWL) and skin hydration (HYDR) assessments were determined on wk 3, 7, and 11 (Phase I) and wk 11, 12, 15, 19, and 23 (Phase II) using a Tewameter[trademark] and Corneometer[trademark] respectively. Blood samples were collected on d 0, 5, 8, 16, 28, 56, and 84. Profiles of plasma phospholipid fatty acids were determined at each collection period. Serum zinc concentrations were analyzed on wk 12, 14, and 24. The hypothesis was that a diet containing increased LA, ALA, and zinc concentrations (diet C) would show improvements of skin and hair coat condition in dogs compared to the other diets. All three test diets caused significant improvements compared to Ol'Roy[trademark]. Diet B caused more improvement than diet A in both subjective and objective assessments of skin and hair coat. Based on mean values diet B is better to be fed to dogs that need to improve skin hydration and diet C should be fed to dogs that need to decrease TEWL. Diet C not only led to improvements in skin and hair coat condition, but also provided additional benefit by producing less pro-inflammatory conditions in the skin.

Diss. (sammanfattning) Uppsala : Sveriges lantbruksuniversitet, 2009. / Härtill 5 uppsatser.

Conjugated linoleic acid (CLA) is produced in the rumen by isomerization of linoleic acid and has been shown to be anticarcinogenic. The objective of this study was to determine the effects of feeding dietary CLA to pre-ruminant lambs or linoleic acid-rich safflower oil to weaned ruminating lambs. Fat content, CLA content and fatty acid (FA) composition of diaphragm, leg, rib, subcutaneous (SC) adipose and liver tissues were determined. The triacylglycerol (TAG) fractions of the total lipid (TL) from the diaphragm, rib and SC adipose tissues were analyzed for FA composition and FA positional distribution. The phospholipid (PL) fractions of the TL were analyzed for FA composition. The positional (PL) fractions of the TL were analyzed for FA composition. The positional distribution of FAs of liver PL was determined. Tissue fat content was affected by diet only in SC adipose tissue. Dietary supplementation with safflower oil increased the fat content of the subcutaneous adipose tissue whereas CLA supplementation resulted in decreased (P<0.05) fat content. Dietary supplementation with safflower oil increased (P<0.05) the CLA content of tissues by more than 200% whereas dietary supplementation with CLA did not affect CLA content. Positional distribution analysis indicated that CLA tends was localized to the sn-1/3 positions of TAG and the sn-2 position of the liver PL. / xiii, 74 leaves : ill. ; 28 cm.

No description available.

The putative peroxisome proliferator-activated receptor (PPAR) α ligand, conjugated linoleic acid (CLA) induced cytoplasmic lipid droplet (LD) formation in H4IIE rat hepatoma cells. Currently, the mechanism(s) by which CLA isomers affects hepatic LD formation is unclear. We have investigated the role of PPARα and fatty acid (FA) activation in the regulation of hepatic LD formation induced by CLA isomers [cis-9,trans-11 (c9,t11), trans-10,cis-12 (t10,c12)] and linoleic acid (LA) in an in vitro model of lipid accumulation. Dose response of c9,t11 and t10,c12 CLA isomers as well as LA in quiescent H4IIE cells was assessed by Oil Red O staining and subsequent quantification after 24 hours. LD formation was induced by the CLA isomers similar to LA in a dose-dependent manner. However, treatment with the acyl CoA synthetase (ACS) inhibitor, triacsin C, resulted in significantly reduced LD formation. A similar reduction in lipid accumulation was observed with the PPARα activator, Wy14643. Furthermore, CLA isomers promoted H4IIE viability at 60 µM but decreased viability at a higher dose of 180 µM. To further understand the role of PPARα in hepatic steatosis, we studied the level and phosphorylation of PPARα in livers of male lean and fa/fa Zucker rats fed either a control diet or fa/fa Zucker rats fed a CLA isomer (0.4% wt/wt c9,t11 or 0.4% wt/wt t10,c12) diet for 8 weeks. Immunoblotting results showed that only the t10,c12 CLA isomer significantly reduced phospho-PPARα S21 compared to the lean control (ln Ctl) and it was associated with a significant increase in the phosphorylation of p38 mitogen activated protein kinase (MAPK).These changes were not observed with the c9,t11 CLA isomer. Taken together, we have shown that CLA isomers directly induce LD formation in quiescent H4IIEs by activation of the lipid storage pathway which was significantly reduced by triacsin C or Wy14643. Also, we demonstrate for the first time that only the t10,c12 CLA isomer significantly reduced PPARα phosphorylation while it increased p38 MAPK phosphorylation. These results indicate that the anti-steatotic effects of the t10,c12 CLA isomer is associated with changes in PPARα phosphorylation and thereby its activity in a MAPK-independent manner.

Endothelial inflammation is a pivotal early event in the development of atherosclerosis. Long term exposure to cardiovascular risk factors will ultimately exhaust those protective anti-inflammatory factors such as the heme oxygenase (HO) system. The HO system plays a critical role in cellular and tissue self-defense against oxidative stress and inflammation. Caveolae are membrane domains and are particularly abundant in endothelial cells, where they are believed to play a major role in the regulation of endothelial vesicular trafficking as well as the uptake of lipids and related lipophilic compounds, possibly including bioactive food components such as flavonoids. Research in this dissertation addresses the role of HO-1 and caveolae on dietary flavonoid epigallocatechin gallate (EGCG) mediated protection against pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) and linoleic acid-induced activation of endothelial cells. The data support the hypothesis that EGCG protects against TNF-α-induced monocyte recruitment and adhesion partially through the induction of HO-1 and bilirubin. The observed anti-inflammatory effects of EGCG are mimicked by the HO-1 inducer cobalt protoporphyrin (CoPP) and abolished by HO-1 gene silencing. Nrf2 is the major transcription factor of phase II antioxidant enzymes including HO-1. Results clearly show that EGCG-induced HO-1 expression and subsequent bilirubin productions are dependent on functional Nrf2. EGCG also can down-regulate the base-line level of caveolin-1. Furthermore, silencing of the caveolin-1 gene can markedly down-regulate linoleic acid-induced COX-2 and MCP-1, indicating that caveolae may be a critical platform regulating inflammatory signaling pathways. Similar to EGCG treatment, silencing of caveolin-1 can also result in the activation of Nrf2, up-regulation of HO-1 and bilirubin. This may be one of the mechanisms to explain the protection effect of caveolin-1 gene silencing against endothelial inflammation. Moreover, EGCG rapidly accumulates in caveolae, which is associated with caveolin-1 displacement from the plasma membrane towards the cytosol. Caveolin-1 gene silencing can significantly reduce the uptake of EGCG in endothelial cells within 30 min. These data suggest that caveolae may play a role in the uptake and transport of EGCG in endothelial cells. These studies provide a novel target through which EGCG functions to protect against inflammatory diseases such as atherosclerosis.

The putative peroxisome proliferator-activated receptor (PPAR) α ligand, conjugated linoleic acid (CLA) induced cytoplasmic lipid droplet (LD) formation in H4IIE rat hepatoma cells. Currently, the mechanism(s) by which CLA isomers affects hepatic LD formation is unclear. We have investigated the role of PPARα and fatty acid (FA) activation in the regulation of hepatic LD formation induced by CLA isomers [cis-9,trans-11 (c9,t11), trans-10,cis-12 (t10,c12)] and linoleic acid (LA) in an in vitro model of lipid accumulation. Dose response of c9,t11 and t10,c12 CLA isomers as well as LA in quiescent H4IIE cells was assessed by Oil Red O staining and subsequent quantification after 24 hours. LD formation was induced by the CLA isomers similar to LA in a dose-dependent manner. However, treatment with the acyl CoA synthetase (ACS) inhibitor, triacsin C, resulted in significantly reduced LD formation. A similar reduction in lipid accumulation was observed with the PPARα activator, Wy14643. Furthermore, CLA isomers promoted H4IIE viability at 60 µM but decreased viability at a higher dose of 180 µM. To further understand the role of PPARα in hepatic steatosis, we studied the level and phosphorylation of PPARα in livers of male lean and fa/fa Zucker rats fed either a control diet or fa/fa Zucker rats fed a CLA isomer (0.4% wt/wt c9,t11 or 0.4% wt/wt t10,c12) diet for 8 weeks. Immunoblotting results showed that only the t10,c12 CLA isomer significantly reduced phospho-PPARα S21 compared to the lean control (ln Ctl) and it was associated with a significant increase in the phosphorylation of p38 mitogen activated protein kinase (MAPK).These changes were not observed with the c9,t11 CLA isomer. Taken together, we have shown that CLA isomers directly induce LD formation in quiescent H4IIEs by activation of the lipid storage pathway which was significantly reduced by triacsin C or Wy14643. Also, we demonstrate for the first time that only the t10,c12 CLA isomer significantly reduced PPARα phosphorylation while it increased p38 MAPK phosphorylation. These results indicate that the anti-steatotic effects of the t10,c12 CLA isomer is associated with changes in PPARα phosphorylation and thereby its activity in a MAPK-independent manner.

Made available in DSpace on 2014-06-11T19:30:30Z (GMT). No. of bitstreams: 0 Previous issue date: 2007-11-30Bitstream added on 2014-06-13T20:40:32Z : No. of bitstreams: 1 andrade_vxl_dr_jabo.pdf: 876282 bytes, checksum: 809d626e35b8733cf7a4cc806ccbed4e (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / O presente trabalho objetivou investigar o efeito da adição de de óleo de milho em dietas com diferentes níveis de proteína bruta, para o pintado, Pseudoplatystoma corruscans, no processo de maturação dos gametas quando mantidos em tanques-rede. Para isso foram avaliados: sobrevivência, relação peso vs comprimento, fator de condição e índice gonadossomático. Além dos índices plasmáticos (colesterol, triglicerídeos, lipídios e proteínas totais e ácidos graxos livres) e o perfil de ácidos graxos nos tecidos dessas matrizes. O experimento foi realizado no Pólo Regional, APTA, Pariquera- Açu, SP, de mar/04 a fev/06. Os tratamentos foram: T1: 28% PB; T2: 28% PB + 5% óleo e T3: 40% PB. As dietas não afetaram a qualidade da água nem o crescimento nos 1º e 2º anos de vida. As taxas de sobrevivência foram superiores a 77%. As rações ofertadas não alteraram o processo de maturação gonadal da espécie. Os peixes apresentaram valores elevados de colesterol, triglicerídeos e lipídios totais, quando acondicionados, justificado pelo fato dos animais estarem se adaptando às novas condições. Essa adaptação também levou a um consumo inicial da fração neutra dos SFA nos tecidos, exceto o adiposo. O óleo à dieta provocou aumento nos teores de PUFA n-6 (incluindo o AA) no músculo das fêmeas, importante reserva energética na atividade migratória. Os HUFA e o LA foram incorporados, preferenciamente aos TGs ovarianos, evidenciando função energética aos ovócitos em formação. Fêmeas estão elongando e desaturando os ácidos graxos para formar AA (a partir do LA), DHA e EPA (a partir do LnA). O estudo indicou que a ração de 28% PB, precisa de mais n-3, preferencialmente EPA e DHA em sua composição, uma fez que foram baixos seus teores nos músculo e fígado o que poderiam ter sido mobilizados aos ovócitos em formação ao final da maturação. / The present work aimed to investigate the effect of the addition of C18:2n6, through the corn oil inclusion in diets with different meaning of crude protein, of the surubim, Pseudoplatystoma corruscans, on the process of gamet maturation, for fish maintained in cages. The experiment was conducted in Regional Polo, Pariquera-Açu, SP, mar./04 to feb./06, whith 12 cages distributed in six tanks, with 20 fishes per cage. It was elaborated three treatments, being two repetitions/tank: T1: 28% CP; T2: 28% CP + 5% corn oil and T3: 40% CP. The diets seems not to have affected the water’s quality neither the growth in the 1st and 2nd years old, with a growth superior lightly of the fish of T3. The survival rates were superior to 77%. It can be inferred that the offered diet did not cause hystomorfologic alterations during the process of gonadal maturation of this species. However, the index gonadossomático (IGS) and the condition factor (K) were slightly advanced and superior in the animals fed with the diet enriched with corn oil.