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The objective of this study was to evaluate the effect of aflatoxin and fumonisin on the performance and health status of Litopenaeus vannamei juveniles and the efficiency of an anti mycotoxin additive (AMA). A 42-day trial with of six treatments and four replicates: (CONT - diet without mycotoxins or AMA, CETX - diet with the addition of AMA, AFLA - diet contaminated with 1067.8 ng/g Aflatoxins, FUMO - diet contaminated with 1715.3 ng/g Fumonisins, AETX - diet with addition of Aflatoxins and AMA; FETX - diet with addition of Fumonisins and AMA). The replicates were randomly assigned to 24 aquaria with individual biological filters. Water quality was monitored for temperature, pH, dissolved oxygen, nitrogenous compounds, alkalinity, hardness and salinity. At the end of the experiment all animals were counted and weighed individually to determine survival (%), mean final weight (g), biomass gain (g) and specific growth rate (%). The hepatopancreas of 16 animals per treatment were collected to perform histopathological evaluation. For water quality variables there is no differences among treatments. Survival was high (>90%) with no significant differences between treatments. For all other performance parameters significant differences were observed due to contamination. Feeding shrimp an aflatoxin or fumonisin contaminated diet resulted in reduced weight, biomass gain, and specific growth rate. The addition of an anti mycotoxin additive compensated these losses and even resulted in significant better growth for the fumonisin contaminated group. Histological damage was observed in all contaminated treatments, although the damage was less pronounced in the treatments containing the anti mycotoxin additive. Results from this study suggest that aflatoxins and fumonisins negatively affect growth and performance of shrimp and that this tested anti mycotoxin additive has proven efficacy in compensating these losses.

New Findings What is the central question of this study? Prenatal protein undernutrition by albumen removal in an avian model of fetal programming leads to long-term programming effects, but when do these effects first appear and are these programming effects regulated by the same candidate genes as in mammals? What is the main finding and its importance? The present results indicate that prenatal protein undernutrition by albumen removal induces phenotypical and hormonal changes in the early posthatch period, when the mismatch between the prenatal and postnatal environment first arises, but these changes are not accompanied by an altered gene expression of the selected candidate genes. Studies of the chicken offer a unique model for investigation of the direct effects of reduced prenatal protein availability by the partial replacement of albumen with saline in eggs at embryonic day 1 (albumen-deprived group). The results were compared with mock-treated sham chicks and non-treated control chicks. Although no differences in hatch weight were found, body weight and growth were reduced in the albumen-deprived chicks until 3 weeks of age. The feed intake of the albumen-deprived chicks, however, was increased compared with the control (day 13–21) and the sham chicks (day 16–18). In the albumen-deprived chicks, the ratio of thyroxine to 3,5,3′-triiodothyronine in the plasma was increased compared with the control chicks, whereas the plasma corticosterone level was increased only at day 7 compared with both other groups. The plasma glucose concentration and glucose tolerance were not affected by treatment. Several candidate genes previously associated with effects of prenatal protein deprivation in mammals were examined in the liver of newly hatched chicks. Gene expression of glycogen synthase 2, glycogen phosphorylase 1, peroxisome proliferator-activated receptor α and γ and glucocorticoid receptor was not affected by the treatment. In conclusion, reduction of prenatal protein availability led to differences in body weight and influenced hormones involved in metabolism and growth. Gene expression of the selected candidate genes was not altered, in contrast to mammals.

To examine the relationship of insulin and glucose, broiler embryos were subjected to acute or prolonged hypoglycemia during the late embryonic phase by, respectively, injecting once (at embryonic day [ED] 16 or 17) or on 3 consecutive days (ED 16, 17, and 18) with tolbutamide (80 μg/g embryo weight), a substance that stimulates insulin secretion from the pancreas. After 1 tolbutamide injection, a prolonged (32 h) decrease of plasma glucose and a profound acute increase in plasma insulin were observed. The 3 consecutive tolbutamide injections induced hypoglycemia for 4 days (from ED 16 to ED 19). The postnatal performance after 3 consecutive tolbutamide injections in broiler embryos was also investigated. Body weight was lower in tolbutamide-treated chickens from hatch to 42 d compared with sham (P = 0.001) and control (P0.001) chickens. Feed intake was lower in the tolbutamide group from hatch to 42 d as compared with sham (P = 0.007) and control (P = 0.017) animals. In addition, at 42 d, plasma glucose concentrations, after an insulin injection challenge (50 μg/kg body weight), were higher in tolbutamide-treated chickens compared with the sham and the control group as were their basal glucose levels (P value of group effect0.001). In conclusion, tolbutamide treatment during the late embryonic development in broilers resulted in prolonged hypoglycemia in this period and negatively influenced the posthatch performance.

Breeder age and nutrition are amongst the most important factors affecting progeny growth and development. The present experiment was carried out to evaluate the effects of n-3 fatty acid (FA), with special emphasis on the ratio of eicosapentaenoic (EPA, 20:5 n-3) and docosahexaenoic (DHA, 22:6 n-3) acid, provided to the diet of ageing broiler breeder hens at different ratios, on the incubation parameters and the performance of the offspring. Four hundred and eighty Ross-308 broiler breeder hens were fed one of four different diets (120/treatment), with an equal fat content. The control diet was a basal diet, rich in n-6 FAs (CON). Blends of fish oil were used to enrich the three other diets in n-3 FA and to obtain different EPA/DHA ratios of 1/1 (EPA=DHA), 1/2 (DHA) or 2/1 (EPA). Every 5 weeks, incubation parameters were assessed. Every 15 weeks, offspring was reared until slaughter age on a standard diet. Breeder age affected almost all incubation and post-hatch parameters, whereas n-3 FA treatment only lowered egg weight (p < 0.0001) and consequently hatched chick weight (p < 0.0001). Supplementation of EPA resulted in a higher proportional liver weight (p = 0.0219) at hatch, a lower body weight up to 28 days post-hatch (p = 0.0418), a lower daily weight gain (p = 0.0498) and a higher feed conversion ratio (p = 0.0395) during the starter period (p = 0.0498), resulting in a higher overall offspring feed conversion ratio (p = 0.0317) compared to the control diet. DHA supplementation, on the other hand, resulted in a lower residual yolk weight (p = 0.0220) and a higher overall offspring mortality (p = 0.0125). In conclusion, supplementation of n-3 FA could not counter the adverse effect of breeder flock age, but did not harm incubation or improve post-hatch performance, either. EPA and DHA affected offspring development differently during early post-hatch life.

The aim of the present study was to investigate whether the immune response of broiler chickens is modulated by including different omega-3 (ω-3) polyunsaturated fatty acids (PUFAs) in the maternal diet. Broiler breeder hens (n = 120 birds per group) were fed one of four diets, differing in the ratios of n-6:n-3 PUFAs and eicosapentaenoic acid (EPA):docosahexaenoic acid (DHA). At 28 weeks of age, the eggs produced were incubated to obtain 720 chicks (n = 180 per group). All broiler chicks were fed a control diet and were vaccinated against Newcastle disease virus (NDV). Blood samples were taken at different time points after immunisation with human serum albumin (HuSA) in Freund's adjuvant to determine the acute phase response, antibody response and cytokine production. Addition of EPA to the maternal diet was associated with greater ovotransferrin concentrations post-immunisation, compared to other groups. Altering the ratios of n-6:n-3 PUFA or EPA:DHA in the maternal diet did not affect the offspring in terms of production of caeruloplasmin, α1-acid glycoprotein, interleukin (IL)-1β, IL-6, IL-12 or tumour necrosis factor (TNF)-α. Dietary manipulation of the maternal diet did not influence the specific antibody response to HuSA or NDV, nor did it alter the levels of natural antibody binding to keyhole limpet haemocyanin in the offspring. Thus, maternal supplementation with n-3 PUFAs played a minor role in perinatal programming of the immune response of broiler chickens.

When added to the feed of broiler breeder hens, dietary polyunsaturated fatty acids (FA) can be incorporated into the yolk and therefore become available to the progeny during their early development. The mechanism involved in lipid metabolism and deposition in the egg may be influenced by breeder age. Before the effect of an elevated concentration of certain polyunsaturated FA on the embryo can be investigated, the effect at breeder level and egg quality must be further assessed. The aim of the present experiment was to evaluate the effects of dietary n-6/n-3 ratios and dietary eicosapentaenoic acid (EPA, 20:5 n-3) and docosahexaenoic acid (DHA, 22:6 n-3) ratios, provided to broiler breeder hens, in terms of their zoo technical performance, egg quality, and yolk FA composition. Starting at 6 wk of age, 640 Ross-308 broiler breeder hens were fed 1 of 4 different diets. The control diet was a basal diet, rich in n-6 FA. The 3 other diets were enriched in n-3 FA, formulated to obtain a different EPA/DHA ratio of 1/1 (EPA = DHA), 1/2 (DHA), or 2/1 (EPA). In fact, after analysis the EPA/DHA ratio was 0.8, 0.4, or 2.1, respectively. Dietary EPA and DHA addition did not affect the performance of the breeder hens, except for egg weight. Egg weight was lower (P < 0.001) for all n-3 treatments. Dietary EPA improved number of eggs laid in the first 2 wk of the production cycle (P = 0.029). The absolute and relative yolk weight of eggs laid by EPA = DHA fed hens was lowest (P = 0.004 and P = 0.025, respectively). The EPA and DHA concentrations in the yolk were highly dependent on dietary EPA and DHA concentrations with a regression coefficient equal to 0.89. It can be concluded that dietary EPA and DHA can be incorporated in the breeder egg yolk to become available for the developing embryo, without compromising the performance and egg quality of the flock.

It is not rare that newly hatched chicks remain without feed for about 24 to 48 h before they are placed on farms due to a series of logistic operations. Furthermore, the spread in hatching time can also mount up to 30 to 48 h for late v. early hatchers. In other words, the practice is a complex combination of spread of hatch and delayed feed access. The present study was aimed to investigate the combined effects of hatching time with a delay in feed access of 48 h, starting from their hatch-time (biological age). When chicks had access to feed immediately after hatch, late hatchers had a higher feed intake and relative growth rate up to day 5 compared with their early hatched counterparts. Feed deprivation during the first 48 h resulted in retarded early growth rate, which was further aggravated by an impaired feed intake after refeeding. In addition, the differential effects of hatching time on relative growth rate and feed intake observed in immediately fed chicks were eliminated by the 48 h feed delay. The yolk utilization after hatch was faster for the late hatchers up to biological day 2 regardless of the feeding treatments. Hatching muscle glycogen content was higher in the late hatchers compared with that of their early counterparts at hatch and at biological day 2 independent of feeding treatment. Moreover, the liver glycogen content of the late hatchers was also higher at hatch. For the immediately fed chicks, the proportional breast muscle weight of the late hatchers was higher at biological day 2 and 5. For the starved chicks, on the other hand, this effect was only observed after they had access to feed (biological day 5). The different plasma T3 levels at hatch may have contributed to the different post hatch performance. It is concluded that the spread of hatch influenced post hatch performance, especially appetite and growth at least until day 5. Moreover, the delay in feed access interacted with the hatching time and caused adverse effects on the post hatch performance.

To examine the importance of albumen as a protein source during embryonic development on the posthatch performance of laying hens, 3 mL of the albumen was removed. At hatch, no difference in BW could be observed. Chicks from the albumen-deprived group had a lower residual yolk weight due to higher yolk utilization. During the rearing phase (hatch to 17 wk of age), the BW of the albumen-deprived pullets was lower compared with the control and sham pullets. The feed intake of the albumen-deprived pullets was also lower than the control pullets. However, during the laying phase (18 to 55 wk of age) these hens exceeded the control and sham hens in BW, although this was not accompanied by a higher feed intake. The albumen-deprived hens exhibited a lower egg production capacity as demonstrated by the reduced egg weight, laying rate, and egg mass and increased number of second grade eggs. In addition, the eggs laid by the albumen-deprived hens had a higher proportional yolk and lower proportional albumen weight. In conclusion, prenatal protein deprivation by albumen removal caused a long-lasting programming effect, possibly by differences in energy allocation, in favor of growth and maintenance and impairing reproductive performance.

The aim of this experiment was to investigate the effect of n-3 fatty acid (FA) supplemented diets on breeder performance, productivity and egg quality. Breeders (n = 480) were fed the supplemented diet from 18 weeks onwards; the inclusion level of n-3 FA was increased from 1.5% to 3.0% from 34 weeks of age onwards until 48 weeks of age. Ross-308 broiler breeders (n = 480) were fed one of four different diets: a basal diet rich in n-6 FA (control diet) or one of three diets rich in n-3 FA. For the n-3 FA diets, eicosapentaenoic acid (EPA, 20:5 n-3) and docosahexaenoic acid (DHA, 22:6 n-3) were fed to the broiler breeders at different ratios formulated to obtain EPA/DHA ratios of 1/1, 1/2 or 2/1. Differences in performance, reproduction and egg quality parameters due to n-3 supplementation were noted more for the 1.5% followed by the 3.0% fed broilers than their 1.5% supplemented counterparts. Egg weight (p

What is the central question of this study? Prenatal protein undernutrition by albumen removal in an avian model of fetal programming leads to long-term programming effects, but when do these effects first appear and are these programming effects regulated by the same candidate genes as in mammals? What is the main finding and its importance? The present results indicate that prenatal protein undernutrition by albumen removal induces phenotypical and hormonal changes in the early posthatch period, when the mismatch between the prenatal and postnatal environment first arises, but these changes are not accompanied by an altered gene expression of the selected candidate genes. Studies of the chicken offer a unique model for investigation of the direct effects of reduced prenatal protein availability by the partial replacement of albumen with saline in eggs at embryonic day 1 (albumen-deprived group). The results were compared with mock-treated sham chicks and non-treated control chicks. Although no differences in hatch weight were found, body weight and growth were reduced in the albumen-deprived chicks until 3 weeks of age. The feed intake of the albumen-deprived chicks, however, was increased compared with the control (day 13-21) and the sham chicks (day 16-18). In the albumen-deprived chicks, the ratio of thyroxine to 3,5,3'-triiodothyronine in the plasma was increased compared with the control chicks, whereas the plasma corticosterone level was increased only at day 7 compared with both other groups. The plasma glucose concentration and glucose tolerance were not affected by treatment. Several candidate genes previously associated with effects of prenatal protein deprivation in mammals were examined in the liver of newly hatched chicks. Gene expression of glycogen synthase 2, glycogen phosphorylase 1, peroxisome proliferator-activated receptor α and γ and glucocorticoid receptor was not affected by the treatment. In conclusion, reduction of prenatal protein availability led to differences in body weight and influenced hormones involved in metabolism and growth. Gene expression of the selected candidate genes was not altered, in contrast to mammals.

In mammalian models of prenatal undernutrition the maternal diet is manipulated, exerting both nutritional and hormonal effects on the offspring. In contrast, in the chicken, strictly nutritional effects can be applied. Prenatal protein undernutrition in chickens was induced by partial replacement of albumen with saline during early embryonic development (albumen-deprived group) and results were compared with a sham-manipulated and a non-manipulated group. Body weight of the albumen-deprived hens was reduced throughout the entire experimental period (0-55 weeks). The reproductive capacity was diminished in the albumen-deprived hens as reflected in the reduced number of eggs and lower egg weight. The plasma triiodothyronine levels were increased in the albumen-deprived group compared with the non-manipulated hens, but not the sham-manipulated hens. An oral glucose tolerance test (OGTT) at 10 weeks of age revealed a decreased glucose tolerance in the albumen-deprived hens. During adulthood, an age-related loss of glucose tolerance was observed in the hens, leading to disappearance of treatment differences in the OGTT. The offspring of the albumen-deprived hens (PA chicks) had reduced body weight until at least 3 weeks of age. In addition, the PA chicks had a decreased relative residual yolk weight at hatching. An insulin tolerance test revealed increased sensitivity to insulin for the PA chicks compared with the offspring of the non-manipulated (PN) and sham-manipulated hens (PS). In conclusion, prenatal protein undernutrition by albumen removal caused long-term effects on body weight, reproductive performance, and physiology. ispartof: Journal of Endocrinology vol:225 issue:2 pages:89-100 ispartof: location:England status: published

The aim of the present study was to evaluate the transfer of maternal dietary fatty acids (FA) from the yolk to the developing offspring, with special emphasis on n-3 FA eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Six hundred forty Ross 308 breeders were housed from 6 to 58 wk of age in 16 pens resulting in 4 replicates per dietary treatment. They were fed 1 of 4 diets: a basal diet, rich in n-6 FA (CON), or an n-3 FA enriched diet formulated to obtain an EPA/DHA ratio of 1/1 (EPA = DHA), 1/2 (DHA), or 2/1 (EPA). At 28, 43, and 58 wk of age, 20 eggs per treatment were collected and analyzed for FA composition. At these same breeder ages, 600 fertilized eggs per treatment were incubated. At hatch the residual yolks of 25 chicks per treatment were collected and analyzed for FA composition. At every hatch, 180 chicks per treatment were raised under standard conditions and livers were sampled at d 1, 14, 28, and 38 d for FA analysis. Concentrations of EPA in the yolk and residual yolk of eggs laid by EPA-fed breeders were highest, next-to-highest for EPA = DHA-fed breeders, next-to-lowest for DHA-fed breeders, and lowest in those laid by control hens, reflecting the inclusion levels in the maternal diets. Yolk and residual yolk DHA concentrations, however, were not only elevated due to DHA supplementation, compared with the control diet, but also due to EPA supplementation. Offspring hepatic EPA concentrations were elevated until d 28 in all n-3 enriched groups, whereas hepatic DHA concentrations were only affected by EPA = DHA and DHA supplementation at d 1. No differences were found in hepatic DHA concentrations at later offspring ages. Considering the role of EPA and DHA in early development and growth, the maternal supply of these n-3 FA might improve offspring health and performance.

Broilers were injected at 10 days of age with either Escherichia coli lipopolysaccharides (LPS) or with Freund's adjuvants (FA) to investigate its triggering effect on the acute phase reaction (APR). First the kinetics of certain APP was studied by sampling blood 4 h, 8 h, 12 h and 24 h post injection with LPS. Ovotransferrin (OVT) and α-1 acid glycoprotein (AGP) concentration increased with time post injection (PI) with LPS to reach a plateau at 12 and 24 h PI. Caeruloplasmin (CP) did not increase with time PI. Compared to injection with phosphate buffered saline, OVT concentrations were higher when injecting chicks with LPS at all time points PI. At 24 h PI, LPS injection resulted in higher OVT and AGP concentration compared to injection with FA. It is recommended to use LPS instead of FA to trigger the APR. The best time point to sample blood for APP determination is 24 h PI.

Chickens have blood glucose concentrations that are twofold higher than those observed in mammals. Moreover, the insulin sensitivity seems to decrease with postnatal age in both broiler and layer chickens. However, little is known about the response of insulin on plasma glucose concentrations and mRNA abundance of hepatic glucose transporters 1, 2, 3, 8, 9 and 12 (GLUT1, 2, 3, 8, 9 and 12) and three regulatory enzymes of the gluconeogenesis, phosphoenolpyruvate carboxykinase 1 and 2 (PCK1 and 2) or fructose-1,6-biphosphatase 1 (FBP1) in chicks during the perinatal period. In the present study, broiler embryos on embryonic day (ED)16, ED18 or newly-hatched broiler chicks were injected intravenously with bovine insulin (1μg/g body weight (BW)) to examine plasma glucose response and changes in hepatic mRNA abundance of the GLUTs, PCK1 and 2 and FBP1. Results were compared with a non-treated control group and a saline-injected sham group. Plasma glucose levels of insulin-treated ED18 embryos recovered faster from their minimum level than those of insulin-treated ED16 embryos or newly-hatched chicks. In addition, at the minimum plasma glucose level seven hours post-injection (PI), hepatic GLUT2, FBP1 and PCK2 mRNA abundance was decreased in insulin-injected embryos, compared to sham and control groups, being most pronounced when insulin injection occurred on ED16.

In contrast to most mammals, chickens have blood glucose concentrations that are twice as high as these in mammals. In addition, they develop a resistance to insulin early in life (Mc Cormick et al., 1978; Seki et al., 2001) So far, the response of insulin to elevated glucose levels in embryonic and neonatal chicks is not well documented and the aim is to explore the glucose metabolism by the injection of insulin in the embryonic and neonatal chick.