Effects of dietary glycine supplementation and fish meal on inflammatory responses in broiler chicks.

1. The effect of dietary protein source and glycine (Gly) supplementation on inflammatory responses was investigated using broiler chicks. Birds (7 d of age) were fed on a maize-soybean meal based (CS) diet with or without 20 g fish meal (FM)/kg and/or 10 g Gly/kg for 14 d. 2. Inflammatory responses were assessed by determining changes in the plasma concentrations of nitrate plus nitrite (NO(x)), caeruloplasmin (Cer) and alpha-1 acid glycoprotein (AGP), and changes in the expression of mRNA encoding substances related to the inflammatory response, such as interleukin (IL)-1 beta and -6, tumour necrosis factor like ligand (TL)1A, inducible nitrite synthase (iNOS), interferon(IFN)-gamma, following lipopolysaccharide (LPS) injection. 3. IL-1 beta and TL1A mRNA expression in chicks fed on the FM diet was higher than in chicks fed on the CS diet. 4. Supplementing the CS diet with Gly resulted in smaller increases in the plasma concentrations of NO(x), Cer and AGP after LPS injection than were observed for chicks fed on the CS diet alone. In addition, 2 h after LPS challenge the expression of encoding inflammatory response-related substances was lower in the spleens of those chicks fed on the Gly-supplemented diet than in those fed the CS diet. 5. Supplementation of the FM diet with Gly reduced the plasma AGP concentration and IL-1 beta and TL1A expression. 6. These results suggest that modulation of inflammatory responses by dietary Gly supplementation is affected by dietary composition; Gly supplementation has different effects on the cytokine responses dependent on the diet.

Effect of dietary supplementation of astaxanthin by Phaffia rhodozyma on lipid peroxidation, drug metabolism and some immunological variables in male broiler chicks fed on diets with or without oxidised fat.

1. Effects of dietary supplementation of astaxanthin (Ax) provided from Phaffia rhodozyma on lipid peroxidation, hepatic drug metabolism, antibody titres to sheep red blood cells (SRBC) and splenocyte proliferation to mitogens were determined in male broiler chicks. 2. Chicks, one week old, were given diets with or without oxidised fat (0 or 3.7 meq of peroxide value (POV)/kg diet) and/or Ax (0 or 100 mg/kg diet) for 14 d, ad libitum. 3. Lipid peroxidation, estimated by 2-thiobarbituric acid reactants values in liver, spleen, heart, plasma and hepatic microsomes, were increased by feeding a diet containing oxidised fat (P<0.05) but were not affected by Ax feeding. 4. Cytochrome P-450 contents in hepatic microsome tended to be increased by feeding Ax. 5. Anti-SRBC titre was not affected by oxidised fat or Ax feeding, while plasma immunogloblin (Ig) G concentration was increased by Ax feeding but was not affected by oxidised fat feeding. 6. When chicks were fed on the diet without oxidised fat, Ax enhanced splenocyte proliferation stimulated by both concanavalin A and pokeweed mitogen, while in chicks fed on a diet containing oxidised fat, Ax reduced the proliferation (P<0.01 for Ax and oxidised fat interaction). 7. The results indicated that dietary supplementation of Ax from Phaffia rhodozyma had an impact on T cell proliferation and Ig G production as a part of acquired immunity, but was not effective in preventing lipid peroxidation in male broiler chicks.

Expression of the chicken peroxisome proliferator-activated receptor-gamma gene is influenced by aging, nutrition, and agonist administration.

Peroxisome proliferatior-activated receptor-gamma (PPARgamma) is a transcription factor that modulates lipid and glucose metabolism in mammals. The aim of the present study was to investigate whether chicken PPARgamma is expressed in tissues in a similar manner to mammalian PPAR and whether it is involved in the regulation of lipid metabolism, particularly in the regulation of fat accumulation in adipose tissue and ovaries. In 30-wk-old chickens, PPARgamma mRNA was detected in most tissues that were examined. Of those tissues expressing chicken PPARgamma mRNA, the lowest expression levels were found in adipose tissue, the tissue that in mammals was shown to express the highest levels of PPARgamma mRNA. Chicken PPARgamma mRNA expression in abdominal adipose tissue tended to increase with age, as shown by higher expression levels at 6 wk than at 1 and 2 wk of age. With regard to nutritional modulation, PPARgamma mRNA levels in abdominal adipose tissue were significantly higher in broiler chickens fed for 7 d a diet containing 8% safflower oil (18:2-rich) or linseed oil (18:3-rich) compared with chickens fed a diet containing olive oil (18:1-rich). In contrast, feeding a 3% cholesterol-supplemented diet for 7 d resulted in no changes to adipose PPARgamma mRNA expression. In broiler chickens orally administered troglitazone, a PPARgamma ligand, abdominal fat pad weight and PPARgamma and lipoprotein lipase (LPL) mRNA levels were significantly increased relative to those of control chickens. Levels of PPARgamma mRNA in liver, skeletal muscle, and ovaries were increased with the onset of egg laying, whereas in adipose tissue the level of PPARgamma mRNA was decreased. These findings suggest that PPARgamma plays an important role in the regulation of fat deposition and egg production and the characteristic pattern of PPARgamma mRNA expression may be indicative of specific differences in the lipid and glucose metabolism of chickens compared with mammals.

Sensory pathways and cyclooxygenase regulate mucus gel thickness in rat duodenum.

We previously showed that the duodenal hyperemic response to acid occurs through activation of capsaicin-sensitive afferent nerves with subsequent release of vasodilatory substances such as calcitonin gene-related peptide (CGRP) and nitric oxide. We then tested the hypothesis that similar factors regulate duodenal mucus gel thickness. Gel thickness was optically measured using in vivo microscopy in anesthetized rats. Duodenal mucosae were superfused with pH 7.0 buffer with vanilloid receptor agonist capsaicin, bradykinin, or PGE(2) injection or were challenged with pH 2.2 solution, with or without the vanilloid antagonist capsazepine, human CGRP-(8-37), N(G)-nitro-L-arginine methyl ester, and indomethacin. Other rats underwent sensory ablation with high-dose capsaicin pretreatment. Acid, bradykinin, capsaicin, and PGE(2) all quickly thickened the gel. Antagonism of vanilloid and CGRP receptors, inhibition of nitric oxide synthase, and sensory deafferentation delayed gel thickening, suggesting that the capsaicin pathway mediated the initial burst of mucus secretion that thickened the gel. Indomethacin abolished gel thickening due to acid, bradykinin, and capsaicin. Inhibition of gel thickening by indomethacin in response to multiple agonists suggests that cyclooxygenase activity is essential for duodenal gel thickness regulation. Duodenal afferent neural pathways play an important role in the modulation of cyclooxygenase-mediated physiological control of gel thickness.

Effect of maternal dietary n-3 fatty acids on the accretion of long-chain polyunsaturated fatty acids in the tissues of developing chick embryo.

The effect of maternal diets on the accretion of n-3 and n-6 polyunsaturated fatty acids in the brain and liver tissue of developing chick embryos was investigated. Hens were fed diets containing high (HLNA) or low levels of 18:3n-3 (LLNA). The HLNA diet increased (p < 0.05) the content of the 18:3n-3, 20:5n-3 and 22:6n-3 in the yolk lipids with a concomitant reduction (p < 0.005) in 20:4n-6. Diet and time significantly (p < 0.05) affected the transfer of 22:6n-3 (docosahexaenoic acid, DHA) and 20:4n-6 acid from the HLNA and LLNA yolk lipid. In the brain of HLNA chick embryos, a diet- and time-associated increase (p < 0.05) in the phospholipid content was observed. In the brain of HLNA and LLNA embryos, DHA levels increased (p < 0.05) from day 15 to the day of hatching, with a concomitant reduction (p < 0.05) in the liver. The accretion of arachidonic acid plateaued on day 15 in the brain of HLNA and LLNA embryos.

Effect of dietary ascorbic acid on the hepatic microsomal mixed function oxidase system in liver of chicks treated with Escherichia coli lipopolysaccharide.

We determined whether dietary ascorbic acid (0.3 or 3 g/kg diet) modulates hepatic microsomal mixed function oxidase (MFO) system and plasma alpha 1 acid glycoprotein (AGP) concentration in chicks treated with Escherichia coli lipopolysaccharide (LPS). Injection of LPS (250 micrograms/kg body weight every other day) intraperitoneally for 14 days decreased cytochromes P450 and b, content and NADPH-cytochrome c reductase activity in hepatic microsomes in male broilers. Content of cytochromes P450 and b5 was negatively correlated with plasma AGP concentration. Feeding ascorbic acid partly alleviated the reduction of cytochromes P450 and b5 in males. Plasma AGP concentration also increased with the LPS injection and was partly lowered by feeding ascorbic acid. The results indicate that dietary ascorbic acid modulates the responses of the microsomal MFO system and of plasma AGP concentration against repeated injection of LPS in male broiler chicks.

Sex-related differences of hepatic microsomal mixed function oxidase system and antibody production in broilers implanted with corticosterone and/or fed ascorbic acid.

1. Most of the components of the mixed function oxidase (MFO) in hepatic microsomes were reduced by corticosterone implants, and the degree of the reduction in females and at an older age was greater than those in males and at a younger age. 2. Ascorbic acid (AA) prevented the reduction in the MFO caused by corticosterone implants. 3. The activities of aniline hydroxylase and aminopyrine N-demethylase were enhanced by corticosterone implants regardless of AA supplementation. 4. The activity of NADPH-cytochrome c reductase in male broiler was greater than that in females under normal conditions. 5. Corticosterone implants and dietary AA had less influence on the antibody production, especially to T-cell dependent antigen.

Effect of an antithyroid agent (propylthiouracil) and L-ascorbic acid on mixed-function oxidase and drug metabolism in hepatic microsomes of chickens.

1. The experiments were undertaken to determine if an antithyroid agent (propylthiouracil, PTU) and/or ascorbic acid (AA) affect mixed-function oxidase (MFO) in hepatic microsomes of male broiler chicks. 2. Feeding PTU increased the MFO activity in a dose-related manner. Addition of AA to the PTU-containing diet further increased the content of cytochromes P-450 and b5, but not the activities of NADPH-cytochrome c and NADH-cytochrome b5 reductase, and the drug-metabolizing enzymes. 3. Supplemental AA induced cytochrome b5 rather than cytochrome P-450.

Effects of supplemental ascorbic acid on performance, organ weight and plasma cholesterol concentration in broilers treated with propylthiouracil.

1. Four experiments were conducted to determine if dietary ascorbic acid (AA) affects body weight gain, food intake, organ weights, plasma cholesterol concentration, and ascorbic acid concentration in the plasma and liver of growing male broilers treated with an antithyroidal agent, propylthiouracil (PTU). 2. In the first experiment, 15 mg AA was administered daily into the crop of chicks fed on a diet supplemented with or without PTU (500 mg/kg). Administration of AA reduced plasma cholesterol concentrations in the PTU-treated chicks. 3. In the other three experiments, chicks were given the basal diet or an AA-containing (3 g/kg) diet supplemented with or without PTU (250 mg or 500 mg/kg). Feeding AA partly prevented the decreases in body weight gain, gain:food ratio and weights of the bursa of Fabricius and thymus in chicks fed on the 250 mg/kg PTU diet, and also prevented the increase in plasma cholesterol concentrations in chicks fed on the PTU diet. 4. These results suggest that AA improves the performance of chicks with experimentally induced hypothyroidism.

Dietary selenium status and plasma thyroid hormones in chicks.

Experiments were conducted to study the effect of marginal levels of selenium and vitamin E on plasma thyroid hormones of meattype chicks. Plasma thyroxine (T4) was significantly increased when a semipurified diet was supplemented with either selenium or vitamin E. Triiodothyronine (T3) was also significantly increased by vitamin E and in one experiment with selenium supplementation. No significant increase in these hormones was observed in birds fed a corn-soybean-meal diet supplemented with these nutrients. Plasma corticosterone level was reduced and weight of the bursa of Fabricius increased by selenium or vitamin E supplementation. These nutrients may be necessary for providing the optimum thyroid conditions for activity of thyroid peroxidase.

Effects of force-feeding and dietary cellulose on liver lipid accumulation and lipid composition of liver and plasma in growing chicks.

Changes of content and composition of lipid in liver and plasma affected by force-feeding and dietary cellulose were investigated in 14-day old Single-Comb White Leghorn male chicks. They were given a purified high energy diet (starch-casein diet without fiber) supplemented with or without dietary cellulose. Chicks were fed ad libitum or force-fed the experimental diet. Force-feeding of excess food improved the growth rate of chicks and feed efficiency, but feeding of cellulose did not affect body weight gain and feed efficiency, though a slight improvement in nitrogen retention was observed. Liver weight and lipid content in liver and plasma were markedly elevated by force-feeding, and were markedly depressed by dietary cellulose in the force-fed chicks. It is suggested that changes of liver lipid by force-feeding and dietary cellulose are mainly originated from the changes of triglyceride in the liver lipid. No marked changes were observed in fatty acid composition of abdominal fat and liver lipid in the cellulose-fed chicks. These results suggest that dietary cellulose may affect lipid metabolism in growing chicks.