Subchronic toxicity and reproduction effects of tri-n-butyltin oxide in Japanese quail

A subchronic toxicity/reproduction study was performed in Japanese quails that were fed a diet containing 0, 24, 60, and 150 mg tri-n-butyltin oxide (TBTO) per kg basal diet for 6 weeks. Eggs produced during the 6 weeks of treatment were incubated and hatched, and chicks hatched from eggs collected in weeks 5 and 6 of exposure were reared for 2 weeks. In parent quail, neither diminished food consumption nor any overt toxic or histopathologic signs were observed following exposure to TBTO. A statistically significant decrease in hatchability and increase in percent of chicks found dead in the shell were observed following TBTO exposure at concentrations of 60 and 150 mg/kg food. However, no significant, adverse effects were recorded on total egg production, eggshell thickness and cracked eggs. Blood chemistry parameters of birds measured at the last day of TBTO treatment revealed a statistically significant decrease in serum aspartate aminotransferase (ASAT) enzyme activity among both sexes in all treatment groups. In addition, a statistically significant dose-related decrease in serum calcium level was observed in females only, while serum follicle stimulating hormone (FSH) levels were statistically significantly reduced in male birds in all treatment groups (approximately 50% of the controls).Moreover, a significant decrease in hepatic microsomal 7-ethoxyresorufin (EROD) activity was recorded in females fed 24 and 60 mg TBTO/kg diet and males fed 60 and 150 mg TBTO/kg diet, whereas pentoxyresorufin-o-deetylase (PROD) activity was only significantly decreased in males fed 150 mg TBTO/kg diet. No TBTO related effects were found on serum alanine aminotransferase (ALAT), serum total thyroxine (TT₄), luteinizing hormone (LH) or retinol levels in both sexes. In summary, TBTO affected mainly reproduction in Japanese quail at a dose where no overt toxicity is observed.     

Effect of a mixture of conjugated linoleic acid isomers on growth performance and antibody production in broiler chicks

The effect of dietary conjugated linoleic acid (CLA) isomers mixture on antibody titres against sheep blood erythrocytes (SRBC) and immunoglobulin (Ig) G concentration in plasma was studied in broiler chickens. In experiment 1, male and female broiler chicks (11 d of age, Cobb strain) were fed a diet supplemented with 10 g CLA or 10 g safflower-seed oil/kg diet for 2 weeks. An SRBC suspension (5:100, v/v) in a phosphate buffer was intravenously injected at 18 d of age and a blood sample was taken from the wing vein at 25 d of age. Chicks fed the CLA-supplemented diet had enhanced first antibody titres in plasma to SRBC as compared with those fed the safflower-seed oil-supplemented diet, irrespective of sex differences. In experiment 2, male broiler chicks (8 d of age, Ross strain) were fed a basal diet or a diet containing 10 g CLA/kg diet for 3 weeks. CLA in the CLA diet partially replaced the soyabean oil in the basal diet. The SRBC suspension was intravenously injected at 15 and 25 d of age and a blood sample was obtained at 21 and 29 d of age. The first antibody titres against SRBC were higher in chicks fed the CLA diet than those in chicks fed the basal diet, but the second titres were not. Plasma IgG concentrations in chicks fed the CLA diet were higher than those in chicks fed the basal diet on both sampling days. The results showed that dietary CLA enhanced antibody production in broiler chickens.     

Absorption and excretion of cholecalciferol and of 25-hydroxycholecalciferol and metabolites in birds

The absorption and excretion in vivo of cholecalciferol or 25-hydroxycholecalciferol (25-HCC) were determined in chicks (Gallus domesticus) and turkeys (Meleagris gallopavo). The overall net cholecalciferol or 25-HCC absorption in chicks and cholecalciferol in turkey poults was 66.5 +/- 3.3, 74.9 +/- 3.7 and 83.6 +/- 7.1% of the intake, respectively. The absorption of cholecalciferol or 25-HCC in chicks and turkeys occurred at the upper part of the intestine. 25-HCC, esters and non-polar metabolites of cholecalciferol or 25-HCC, and their polar metabolites, were secreted in the duodenum of chicks and turkeys but were partially reabsorbed at the upper part of the jejunum.     

Oral iodine toxicity in chicks can be reversed by supplemental bromine

Four chick bioassays were conducted to quantify iodine (I) toxicity and its amelioration in young chicks. A supplemental I level from KI of 600 mg/kg depressed growth in chicks fed methionine-deficient diets but not in those fed methionine-adequate diets. An I dose level >or= 900 mg/kg was required to cause growth depression in chicks fed a methionine-adequate corn-soybean meal diet. Iodine intoxicated chicks also displayed neurological symptoms and extreme malaise, but dose levels up to 1200 mg I/kg had no effect on blood hemoglobin or hematocrit. Supplemental I levels of 1000-1500 mg/kg caused severe growth depressions that could be totally reversed by dietary addition of 50 or 100 mg/kg bromine provided as NaBr. Nuclear accidents or terrorist actions that result in I toxicity and thyroid cancer or goiter may benefit from use of NaBr as a therapeutic agent.     

Prevention of immunologic stress contributes to the growth-permitting ability of dietary antibiotics in chicks.

The growth-permitting ability of antibiotics fed to broiler chicks was studied as it relates to the state of activation of the immune system. In Experiment 1, chicks were fed two levels of antibiotics (0 or 100 mg streptomycin + 100 mg penicillin/kg diet) and were raised either in an environment with poor sanitation to create a chronic immune stress or in a clean environment. Chicks raised in the unsanitary environment and not fed antibiotics had significantly lower (P < 0.05) rates of weight gain and efficiencies of feed utilization, and higher levels of plasma interleukin-1, compared with chicks raised in the clean environment or chicks raised in the unsanitary environment and fed antibiotics. Adding antibiotics to the diet of birds in the clean environment did not affect any variable. In Experiment 2, chicks were raised in a conventional environment and fed two levels of an antibiotic (0 or 100 mg tetracycline/kg diet). After a 15-d feeding period, half of the chicks were injected with Salmonella typhimurium lipopolysaccharide to create an acute immunologic stress. Feeding antibiotic resulted in improved weight gain, feed consumption and efficiency of feed utilization. Lipopolysaccharide-injected birds developed heavier livers, spleens and intestines relative to body weights and higher rectal temperatures and hepatic metallothionein concentrations, presumably due to an immunologic stress. Omitting antibiotic from the diet resulted in similar changes. These results indicate that feeding antibiotics may permit growth by preventing immunologic stress and associated metabolic changes brought about by monokines including interleukin-1.     

Amelioration of oral copper toxicity in chicks by dietary additions of ascorbic acid, cysteine and zinc

Four experiments were conducted to evaluate the interrelationship of L-ascorbic acid, L-cysteine and Zn for amelioration of Cu toxicity in chicks. Chicks were fed a corn-soybean meal diet with 1,000 mg Cu (CuSO₄ · 5H₂O)/kg to produce Cu toxicity. Single dietary additions and two-way combinations of ascorbic acid (1,000 mg/kg), cysteine (0.5 g/100 g) and Zn (1,000 mg/kg) reduced liver Cu accumulation, with cysteine resulting in the largest response. Although supplemental Zn from ZnSO₄ · 7H₂O reduced liver Cu concentrations, it also reduced chick weight gain and food intake. Experiment 2 tested a range of cysteine and Zn levels to determine their effects on Cu toxicity in chicks. Supplemental Zn levels as low as 500 mg/kg reduced growth, but a cysteine level as low as 0.1 g/100 g increased chick weight gain and reduced liver Cu. Experiment 3 evaluated two Zn sources to determine if Zn source was affecting weight gain of chicks fed high Cu diets. There was a reduction in chick weight gain with 1,000 mg Zn/kg from Zn sulfate, but no reduction in weight gain with the same level of Zn from Zn oxide. In Experiment 4, 1,000 mg ascorbic acid/kg, 0.05 g/100 g cysteine and 1,000 mg Zn/kg from Zn oxide were tested in a 2 x 2 x 2 factorial. As in Experiment 1, ascorbic acid, cysteine and Zn were all effective in reducing liver Cu. The results suggested that L-cysteine was more effective than either L-ascorbate or Zn in ameliorating Cu toxicity, but a lower dose of cysteine together with pharmacologic additions of ascorbate and Zn (from ZnO) may be just as effective.     

Serum metabolite profiles and target tissue gene expression define the effect of cholecalciferol intake on calcium metabolism in rats and mice

We studied the effect of cholecalciferol (VD3) intake on VD3 status and markers of calcium (Ca) homeostasis in mice and rats. Serum 25 hydroxycholecalciferol (25OH-VD3) concentrations were increased in animals fed diets containing 400-20,000 international units (IU) VD3/kg (37 nmol.L(-1).1000 IU VD3(-1)), but body weight, serum Ca, and duodenal gene expression were not altered. High-VD3 intake decreased serum 1, 25-dihydroxycholecalciferol [1,25(OH)2-VD3] and renal 25 hydroxycholecalciferol-1alphahydroxylase (CYP27B1) mRNA, suggesting that rodents tolerate high-VD3 intake by suppressing the activity of the VD3 endocrine system. Serum 25OH-VD3 declined when animals were fed diets containing 1000 to 25 IU VD3/kg (9-11 wk, inflection at 200 IU/kg, 4-fold steeper slope below this). Neither body weight nor serum Ca were influenced by low-VD3 intake. However, mice fed the 25-IU/kg diet had lower serum 1,25(OH)2-VD3, duodenal calbindin D9k mRNA, bone mineral density, and renal 25 hydroxycholecalciferol-24 hydroxylase mRNA, whereas renal CYP27B1 mRNA was elevated when rodents were fed < 200 IU VD3/kg. These data reveal a stress on VD3 and Ca metabolism at low dietary VD3 intake. Dietary Ca restriction (0.25 vs. 0.5%, 9 wk) increased serum 1,25(OH)2-VD3 and was 30% greater in rats fed a 10,000-IU VD3/kg diet. High-VD3 intake did not prevent Ca restriction-induced bone loss. Our data show that modeling human VD3 status requires lower intake than the current NRC rodent requirement (1000-IU/kg diet). Also, although rodents are very tolerant of high-VD3 intake, it cannot compensate for moderate Ca restriction.     

Effect of level of protein intake on calcium metabolism and on parathyroid and renal function in the adult human male.

Mechanisms involved in the hypercalciuria caused by high levels of protein intake were investigated. Six healthy males participated in a 20-day metabolic study. During the first 10-day period, all subjects were given a 47 g protein diet and during the second 10-day period, a 142 g protein diet. Calcium, magnesium and phosphorus intakes were kept constant at 515, 320 and 1,110 mg daily, respectively. Urinary calcium was elevated significantly when the protein intake was increased. Glomerular filtration rate and calcium clearance were increased significantly when the high protein diet was fed; the fractional tubular reabsorption of calcium was decreased from 98.4 to 97.4%. Thus, the increase in urinary calcium caused by the high protein diet appears to be due in part to an increase in the filtered load of calcium by the glomeruli and in part to a decrease in calcium reabsorption by the renal tubules. The level of protein intake had no effect on the fasting serum concentrations of parathyroid hormone, total calcium, magnesium or inorganic phosphorus or plasma ultrafiltrable calcium.     

Serum calcium, phosphorus and magnesium responses to massive dosing of cholecalciferol (CC) and 25-OH-CC in young and aged ewes

Twenty-four ewes were divided into two age groups (one-year-old and nine-year-old) and used to determine the influence of cholecalciferol (CC) and 25-OH-CC on serum concentrations of Ca, P, and Mg with time post-injection. The ewes were maintained in slatted-floor pens and fed 800 g per head daily of a diet which analyzed 0.38% calcium, 0.31% phosphorus, and 0.14% magnesium. This diet was fed throughout the 21-day trial. The ewes were injected on days 0 and 7 as follows: (control) 5 ml ethanol; (CC) 50 mg CC in 5 ml ethanol; and (25-OH-CC) 25 mg 25-OH-CC in ethanol. Blood samples were pre-injection (day 0) and on days 1, 2, 3, 5, 7, 9, 12, 17 and 21 of the trial. Serum Ca averaged 10.81, 11.06 and 11.25 mg/100 ml for the one-year-old ewes and 10.51, 11.06 and 11.54 mg/100 ml for the nine-year-olds across sampling times in groups A to C, respectively. Serum P across sampling times averaged 6.58, 7.80 and 9.51 mg/100 ml in one-year-old ewes and were different (P less than .05) from each other. Serum P averaged 7.06, 8.56 and 8.59 mg/100 ml for the nine-year-old ewes. Serum Mg values were 2.51, 2.32 and 2.19 mg/100 ml for the one-year-old and 2.38, 2.14 and 2.00 mg/100 ml for the nine-year-old ewes across all sampling times for control, CC and 25-OH-CC groups, respectively. Serum Mg in one-year-old ewes was lower (P less than .05) in both CC and 25-OH-CC injected ewes than controls, and was lowest (P less than .05) for 25-OH-CC when compared with the control in nine-year-old ewes. External symptoms of hypervitaminosis (reduced feed intake and leg abnormalities) were apparent after the second injection with 25-OH-CC, and were most pronounced in the aged ewes.     

Effect of lead and niacin on growth and serotonin metabolism in chicks

Interactions of lead and niacin were studied in growing broiler chicks fed one of four experimental diets from day-old to 3 wk of age. The diets were a low niacin basal diet (LN), the basal diet supplemented with 40 mg of niacin/kg (control), the basal diet supplemented with 2000 mg lead/kg, as lead acetate (LN + Pb) and the basal diet supplemented with both niacin and lead (control + Pb). Growth and feed efficiency were reduced significantly by lead. The lead-associated growth depression was less severe in chicks fed the low niacin diet as indicated by a significant lead X niacin interaction. The relative weights of two brain regions (telencephalon and diencephalon) and the adrenal glands were greater in lead-treated chicks than in their nonlead-treated counterparts. Plasma and telencephalon tryptophan were lower in lead-treated chicks than in nonlead-treated chicks. Diencephalon tryptophan was lower in chicks fed the LN diet than in chicks fed the control diet. Brain serotonin was lower and 5-hydroxyindoleacetic acid was higher in both brain regions of lead-treated chicks than in nonlead-treated chicks. The data indicate that tryptophan and serotonin metabolism were altered by lead treatment, whereas niacin was without effect. The interaction of lead and niacin on growth does not appear to be related to alterations of serotonin metabolism in the central nervous system.     

Medium-chain triacylglycerols enhance release of cholecystokinin in chicks.

Whether medium-chain triacylglycerols (MCT) affect the plasma concentration of cholecystokinin (CCK) and crop-emptying rate in chicks was investigated after 0, 30, 60, 90, 120 or 180 min of diet intubation. Triacylglycerol sources used were corn oil [containing long-chain triacylglycerols (LCT)], glyceryl tricaprate and glyceryl tricaprylate at a level of 200 g/kg diet. Plasma CCK concentration was significantly enhanced in chicks given the two MCT treatments, but not in those given the LCT treatment, after 30 min feeding relative to the initial level. At all time points, chicks fed the diet containing LCT had significantly lower plasma CCK concentrations than those fed MCT, and chicks fed glyceryl tricaprate had higher concentrations than those fed glyceryl tricaprylate. Dietary MCT sources significantly delayed diet passage from the crop compared with dietary LCT. These results indicate that MCT are more potent stimulators of CCK secretion in chicks than LCT.     

A comparison of the effects of dietary calcium and phosphorus deficiency on the in vitro and in vivo metabolism of 25-hydroxycholecalciferol in the chick

1. Young chicks fed a diet deficient in calcium showed an eightfold increase in the in vitro renal production of 1,25-dihydroxycholecalciferol (1,25-DHCC) and those fed a diet deficient in phosphorus showed a threefold increase when compared to chicks on a normal diet. 2. The in vivo accumulation of 1,25-DHCC in the gut mucosa was doubled in both low-Ca and low-P groups as was the rate of Ca absorption from the duodenum and the Ca-binding protein activity. The accumulation of 1,25-DHCC in bone increased threefold in the low-Ca group but showed no change in the low-P group. 3. It was concluded that the increased rate of Ca absorption found in dietary P deficiency depends rather upon the capacity of the gut mucosa to accumulate larger amounts of 1,25-DHCC than upon an increased renal production of this metabolite. The mechanism by which this is achieved is unknown, but it unlikely to be a general increase in availability of 1,25-DHCC since no rise occurred in bone 1,25-DHCC levels.     

Excess dietary L-cysteine causes lethal metabolic acidosis in chicks

A 72-h time-course study was conducted to elucidate the physiological mechanism underlying cysteine (Cys) toxicity in chicks beginning at 8-d posthatch. Biochemical markers quantified in plasma and liver samples collected from chicks receiving 30 g/kg excess dietary Cys were compared with baseline measurements from chicks receiving an unsupplemented corn-soybean meal diet over a 72-h feeding period. Concomitant with chick mortality were indices of acute metabolic acidosis, including a rapid increase (P < 0.001) in anion gap that resulted from a reduction (P < 0.001) in plasma HCO(3)(-) of approximately 40% and a 2.8-fold increase (P < 0.001) in plasma sulfate in chicks receiving excess Cys. Additionally, provision of 30 g/kg excess Cys resulted in a 1.5-fold increase (P < 0.05) in hepatic oxidized glutathione compared with the 0-h control time-point. Excess dietary Cys did not affect plasma free Met, but plasma free Cys increased (P < 0.05) from 89 to 107 mumol/L at 12 h and remained elevated through 36 h. Strikingly, ingestion of 30 g/kg excess Cys caused more than a doubling (P < 0.001) of plasma free cystine, the oxidized form of Cys, beginning 12 h after initiating the study, and it remained elevated throughout the 72-h feeding period. Taken together, these data suggest that ingestion of 30 g/kg excess l-Cys causes both acute metabolic acidosis and oxidative stress in young chicks when fed a nutritionally adequate, corn-soybean meal diet.     

Excess dietary methionine markedly increases the vitamin B-6 requirement of young chicks

A soy-protein isolate diet that contained essentially no bioavailable vitamin B-6 was used to establish the quantitative effect of excess dietary methionine on the vitamin B-6 requirement of young chicks. When made adequate in vitamin B-6, chicks fed the basal diet required 2 g/kg supplemental DL-methionine to achieve maximal growth, and 10 g/kg additional DL-methionine (total = 12 g/kg) was found to be a tolerable excess level that would not depress voluntary food intake or growth rate. When chicks were fed seven graded doses of supplemental pyridoxine (PN) in diets that contained either adequate (2 g/kg) or excess (12 g/kg) methionine, the vitamin B-6 requirement for maximal growth was found to increase (P: < 0.01) from 0.73 to 1.05 mg/kg, a 44% increase, when 10 g/kg excess methionine was present in the diet. Indeed, this level of excess dietary methionine depressed (P: < 0.01) growth at all PN dose levels < or =1 mg/kg, but not at PN doses of 1.2 or 1.4 mg/kg. Because dietary intakes of both vitamin B-6 and methionine can affect plasma homocysteine levels, dietary methionine (and protein) intake should be considered important factors in setting safe and adequate requirement levels for vitamin B-6.     

Involvement of lipoic acid in plasma metabolites, hepatic oxygen consumption, and metabolic response to a beta-agonist in broiler chickens

The present study was conducted to determine the role of alpha-lipoic acid (LA) in plasma metabolites, hepatic O2 consumption, and beta-adrenergic response in broilers. In Expt 1, 12-d-old female broiler chicks were divided into three dietary groups and fed on diets with or without LA (5 or 50 mg/kg) until 4 or 6 weeks of age, as a 2 x 3 factorial arrangement. The dietary LA had no effect on growth rates (body weight, abdominal fat, breast muscle, and liver). The higher level of LA increased plasma non-esterified fatty acid and decreased plasma triacylglycerol concentrations only at 6 weeks of age. A 42% increase in hepatic respiration was observed in the 4-week-old chickens given 50 mg LA/kg diet. In Expt 2, 3-d-old female broiler chicks were treated with or without dietary LA at 50 mg/kg. At 30 and 31 d old, isoproterenol (2 mg/kg body weight per h) was continuously infused into a wing vein for 2 h, and changes in plasma glucose, triacylglycerol, and non-esterified fatty acid concentrations were analysed. Isoproterenol increased plasma glucose over basal levels maximally at 60 min. Furthermore, the glucose increase in the LA-treated chickens was 35% greater than that of the controls at this time. Plasma non-esterified fatty acid and triacylglycerol concentrations were decreased by the isoproterenol infusion, regardless of LA administration. Therefore, the present study suggests that dietary LA has repartitioning effects on energy metabolism in chickens (although this depends on age-related metabolic state) and is a possible facilitator in the beta-adrenergic response of plasma glucose to a beta-agonist.     

Aluminum and Acid Effects on Calcium and Phosphorus Metabolism in Young Growing Chickens (Gallus gallus domesticus) and Mallard Ducks (Anas platyrhynchos)

Acidification is associated with increased mortality, reduced growth, and bone abnormalities in birds. Associated with acid deposition is an increase in aluminum availability due to solubilization from soil and other sources. (Conversely, experimental diets containing aluminum sulfate have much reduced pHs.) The present studies compare the effects of two levels of dietary acid (sulfuric acid) (0.122 and 0.56 mol H⁺ per kg feed; 0.056 and 0.277 mol sulfate per kg feed) and dietary aluminum (aluminum sulfate at 0.1 and 0.5%; sulfate at 0.056 and 0.277 mol sulfate per kg feed) on bone growth, mineralization, and phosphorous/calcium homeostasis in growing birds (chickens and mallard ducks). Growth was reduced by the high acid (chicken) and aluminum (ducks and chickens) diets. A reduction in bone mineralization was observed in birds receiving aluminum-containing diets [low aluminum diet: decreased tibia ash, calcium, and phosphorus (chickens); high aluminum diet: decreased tibia dry weight, % of ash and mg; ash, calcium (chickens, ducks as % of ash), and phosphorus (chickens mg/duck, % of ash)]. Moreover, plasma concentrations of inorganic phosphate were reduced in chicks on the high aluminum diet. There were also marked decreases in bone growth and mineralization [tibia weight, ash (mg), calcium (mg), phosphorus (mg)] and plasma concentrations of 1,25-dihydroxy vitamin D₃ in chicks on the high acid diet compared to those on a control diet. These changes were probably due to reduced feed intake; changes in bone indices being of a greater or similar magnitude in pairfed control. There was little change in bone indices, growth rate or feed consumption in ducklings receiving either the low or high acid diets. It is concluded that aluminum directly adversely affected bone mineralization whereas acid effects are mediated in part by changes in feed consumption. Received: 22 July 1997/Accepted: 29 November 1997     

镁的不同摄入水平对生长期大鼠钙、磷、镁代谢及骨骼的影响

目的　研究饲料缺镁或高镁对生长期大鼠钙、磷、镁吸收代谢以及骨骼发育的影响。方法　 30只 SD大鼠 ,分为三组 ,每组 1 0只 ,单独喂养在有机玻璃代谢笼中 ,第一组大鼠饲喂缺镁饲料 (含镁 86mg/kg) ,第二组饲喂适量镁饲料 (含镁 548mg/kg) ,第三组为高镁饲料 (含镁540 2 mg/kg) ,三组饲料均为人工半合成制备 ,其中含钙 3.7g/kg,含磷 4g/kg。经过 2 5天对喂养方法及代谢笼的适应后 ,开始 5天期的代谢实验。每天记录大鼠的进食量 ,分别收集每个大鼠的粪、尿。代谢实验结束后 ,禁食 1 2 h,在乙醚麻醉下 ,心脏采血并处死大鼠 ,取股骨、胫骨测定重量、长度和体积后 ,与肾脏一起储存于 - 2 0℃ ,待测钙、镁和磷的含量。结果　缺镁和适量补镁对钙的表观吸收基本没有影响 (86% ) ,饲料中过量的镁使大鼠钙的表观吸收略有下降 (83% ) ,高镁使尿钙排出显著增加 ,降低了钙在体内的滞留 ;饲料高镁使磷的表观吸收显著下降。但尿磷排出减少 ,磷在体内滞留反而增加。随着饲料中镁含量的增加 ,粪和尿中镁的排泄均大幅度上升 ,可见镁的内环境稳定由肠道和肾脏共同调节。结论　低镁和高镁饲料均不利于生长期大鼠骨骼的生长发育。低镁饲料使大鼠肾钙、磷蓄积 ,可能是肾结石形成的主要原因。     

Tissue zinc and copper levels in diabetic C57BL/KsJ (db/db) mice fed a zinc-deficient diet: lack of evidence for specific depletion of tissue zinc stores

We investigated whether the decreased femur zinc concentrations reported in genetically obese diabetic db/db C57BL/KsJ mice reflected an increased propensity to zinc deficiency by determining zinc concentrations in tissues from 18-19-wk-old db/db and control mice following ad libitum feeding of a zinc-deficient diet (2 mg/kg) or restricted or ad libitum feeding of a zinc-adequate diet (20 mg/kg) for 12 wk. Although hepatic and renal zinc concentrations of db/db mice fed the zinc-deficient diet tended to be lower than in any other experimental group when expressed on a dry weight basis, zinc concentrations in these tissues were either not different from or greater than those of their nondiabetic controls when expressed on an ash weight basis, i.e., relative to all mineral constituents of these organs. Hepatic and renal copper concentrations of the diabetic db/db mice were either not different from or greater than those of their controls on an ash weight basis. Femur zinc concentrations of diabetic db/db mice fed zinc-adequate diets were lower than those of their controls on a dry weight basis but were not different from their controls on an ash weight basis. We found proportionately lower dry zinc, calcium and magnesium concentrations in femurs of the db/db mice fed a nonpurified diet than in femurs of their db/m and m/m controls. These findings suggest that the low femur zinc concentration reported in the diabetic db/db mouse probably reflects a generalized decrease in bone mineral content rather than a specific depletion of tissue zinc stores.     

Dietary supplementation of glycine modulates inflammatory response indicators in broiler chickens

Three experiments were conducted to investigate the effect of dietary glycine (Gly) supplementation on inflammatory responses in broiler chicks fed a basal diet using maize and soybean meal as the primary ingredients. Inflammation-related processes following lipopolysaccharide (LPS) injection were examined by analysing plasma concentrations of nitrate plus nitrite (NOx) and ceruloplasmin (Cer) in experiments 1 and 2, or expression of several genes in the spleen and liver including IL-1 beta and -6, TNF-like ligand (TL)1A, inducible NO synthase, interferon (IFN)-gamma and toll-like receptor (TLR) 4 were examined in experiment 3. Growth performance was also determined following immunological stimulation by both LPS and Sephadex injection in experiment 2. In experiment 1, birds fed a diet supplemented with Gly at 10 or 20 g/kg showed lower responses in plasma NOx and Cer than birds fed the diet supplemented with Gly at 0 or 40 g/kg. In experiment 2, a similar effect of Gly supplementation at 10 g/kg on plasma NOx and Cer was observed when chicks were fed either an isonitrogenous diet with Gly or glutamic acid (Glu). Gly-supplemented diet-fed birds showed better growth performance than Glu-supplemented diet-fed birds. The splenic expression of inflammatory response-related genes in birds fed a diet supplemented with Gly at 10 g/kg diet was lower than that of birds fed the basal diet in experiment 3. These results suggest that dietary Gly supplementation modulates the inflammatory response partly through changes in the expression of pro-inflammatory cytokines such as IL-1, IL-6, IFN-gamma and TL1A.     

Barley beta-glucans alter intestinal viscosity and reduce plasma cholesterol concentrations in chicks.

Ninety-six 14-d-old male broiler chicks were divided into three dietary groups and fed a corn-soybean meal diet, a barley diet with beta-glucanase and that diet without beta-glucanase. All diets contained 4 g cholesterol/kg. Average daily body weight gain, plasma total cholesterol concentration, LDL cholesterol concentration and digestibility of lipids and protein were lowest (P < 0.05) in the chicks fed the barley diet without beta-glucanase and highest (P < 0.05) in the chicks fed corn-soybean meal diet. Supplementation of the barley diet with beta-glucanase resulted in greater (P < 0.05) average daily weight gain, plasma total and LDL cholesterol concentrations and digestibility of lipids. Viscosity of small intestinal digesta was greatest in chicks fed barley, lowest in those fed the corn-soybean diet and intermediate in chicks fed enzyme-treated barley. Significant (P < 0.01) negative correlations occurred between viscosity of the small intestinal contents and average daily weight gain, plasma total and LDL cholesterol concentrations, and digestibility of lipids and protein. A lower concentration of insoluble beta-glucans in small intestinal digesta of the chicks fed barley supplemented with beta-glucanase compared with the chicks fed the unsupplemented barley diet reflects hydrolytic activity of the supplemental beta-glucanase in the diet.