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        Effects of feed access after hatch and inclusion of fish oil and medium chain fatty acids in a pre-starter diet on broiler chicken growth performance and humoral immunity
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        Effects of feed access after hatch and inclusion of fish oil and medium chain fatty acids in a pre-starter diet on broiler chicken growth performance and humoral immunity
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        Effects of feed access after hatch and inclusion of fish oil and medium chain fatty acids in a pre-starter diet on broiler chicken growth performance and humoral immunity
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Abstract

Delayed feed and water access is known to impair growth performance of day old broiler chickens. Although effects of feed access on growth performance and immune function of broilers have been examined before, effects of dietary composition and its potential interaction with feed access are hardly investigated. This experiment aimed to determine whether moment of first feed and water access after hatch and pre-starter composition (0 to 7 days) affect growth rate and humoral immune function in broiler chickens. Direct fed chickens received feed and water directly after placement in the grow-out facility, whilst delayed fed chickens only after 48 h. Direct and delayed fed chickens received a control pre-starter diet, or a diet containing medium chain fatty acids (MCFA) or fish oil. At 21 days, chickens were immunized by injection of sheep red blood cells. The mortality rate depended on an interaction between feed access and pre-starter composition (P=0.014). Chickens with direct feed access fed the control pre-starter diet had a higher risk for mortality than chickens with delayed feed access fed the control pre-starter diet (16.4% v. 4.2%) whereas the other treatment groups were in-between. BW gain and feed intake till 25 days in direct fed chickens were higher compared with delayed fed chickens, whilst gain to feed ratio was lower. Within the direct fed chickens, the control pre-starter diet resulted in the highest BW at 28 days and the MCFA pre-starter diet the lowest (Δ=2.4%), whereas this was opposite for delayed fed chickens (Δ=3.0%; P=0.033). Provision of MCFA resulted in a 4.6% higher BW gain and a higher gain to feed ratio compared with other pre-starter diets, but only during the period it was provided (2 to 7 days). Minor treatment effects were found for humoral immune response by measuring immunoglobulins, agglutination titers, interferon gamma (IFN- γ ), and complement activity. Concluding, current inclusion levels of fish oil (5 g/kg) and MCFA (30 g/kg) in the pre-starter diet appear to have limited (carryover) effects on growth and development, as well as on humoral immune function.

Implications

Delayed feed intake after hatch for broiler chickens resulted in lower BW gain. Thus, changing hatchery and farm management towards direct feeding after hatch can shorten the growth period. Feeding medium chain fatty acids (MCFA) during the first week after hatch resulted in higher BW gain and improved feed efficiency during the first week after hatch. A shortened growth period, as well as improved growth performance due to feeding MCFA, may result in economic benefits for the farmer.

Introduction

Although commonly accepted in modern broiler farming, a delayed first feed and water intake for chickens due to spread of hatch, handling at the hatchery and transport to the grow-out facility, may impair BW gain and organ growth (Van de Ven et al., 2013; Lamot et al., 2014). Additionally, delayed feed intake was found to result in relatively smaller immune organ sizes up to at least 2 weeks of age (Bar-Shira et al., 2005). Although delayed feed intake seems to have limited effect on (mucosal) immune function in healthy broiler chickens (Simon et al., 2014), it does seem to affect the specific antibody response to an immune challenge in later life and colonization of T and B lymphocytes in the cecum and colon (Bar-Shira et al., 2005).

The effect of delayed feeding on BW gain and immune function may also interact with diet composition. Direct and delayed fed chickens may have different dietary requirements due to their metabolic state and as such diets may skew immune function differently when fed immediately or delayed. Diet composition is also important during the first days after hatch as the gastrointestinal tract is still immature (Christensen, 2009) and enzyme secretion is not fully functional. Thereby, nutrient digestibility during the first week after hatch is not optimal yet and needs to be accounted for.

While the role of protein and amino acids in pre-starter diets has been studied extensively (Wijtten et al., 2010), studies on the use of dietary fat are limited due to the general perception that fats are not well digested at that age (Batal and Parsons, 2002; Thomas et al., 2008). However, these fats and oils might have an effect on immune function. Two profound examples are fish oil (rich in n-3 long chain polyunsaturated fatty acids) and medium chain fatty acids (MCFA). Fish oil has been found to reduce inflammatory responses at 2 weeks of age when fed to broilers (Korver and Klasing, 1997). On the contrary, MCFA (especially lauric acid; C12:0) were found to increase IL-1α expression in vitro in a dose response manner through toll-like receptor (TRL-4) activation (Lee et al., 2001). Although effects of nutrition on immune function in poultry have been extensively reviewed (Korver, 2012), most studies do not focus on effects of nutrition in the 1st week after hatch. Moreover, mostly general effects of feed and water access on immune function and function are studied, ignoring effects of diet composition (Walstra, 2011; Simon et al., 2014).

The current experiment aimed to determine whether (1) moment of feed and water access after hatch and (2) pre-starter composition affected growth rate and innate and specific humoral immune function in broiler chickens until 28 days. It is hypothesized that inclusion of fish oil or MCFA in a pre-starter diet will result in higher BW gain and feed efficiency and altered humoral immune function.

Material and methods

The procedures applied in this experiment were approved by the Animal Care and Use Committee of the Animal Sciences Group of Wageningen University and Research Centre, the Netherlands.

Experimental design and diets

Effects of moment of first feed and water access (for the remainder referred to as ‘feed access’), and pre-starter composition were studied using a 2×3 factorial arrangement of treatments. Direct fed chickens received feed access directly after placement in the grow-out facility, wheras delayed fed chickens were withheld from feed access for 48 h after placement onward. Pre-starter diets contained either soybean oil (control), fish oil at 5 g/kg diet, or a MCFA blend at 30 g/kg diet (3 g/kg diet C10:0 and 27 g/kg diet C12:0; Sigma-Aldrich Chemie B.V., the Netherlands). Fish oil and MCFA were exchanged against soybean oil to keep the diets isocaloric. Pre-starter diets (2.0 mm pellet; 0 to 7 days) were followed by a starter (2.5 mm pellet; 7 to14 days) and grower diet (3.0 mm pellet; 14 to 28 days) that were similar for all treatment groups. Diets were formulated based on digestibility and nutrient data provided by CVB (2007), the compositions of the pre-starter, starter and grower diets are provided in Table 1. Pre-starter diets were manufactured using one basal diet and together with starter and grower diets produced and pelleted by Research Diet Services (the Netherlands). All chicken were fed ad libitum from the moment of feed access till the end of the experiment. At 21 days, all chickens were immunized by injection in the pectoralis major with 1.0 ml of 25% volume-based sheep red blood cells (SRBC) suspension in phosphate-buffered saline.

Table 1 Ingredient and nutritional composition of the experimental diets

MCFA=medium chain fatty acids.

1 Sigma-Aldrich Chemie B.V., the Netherlands.

2 Contributed per kilogram of diet: vitamin A, 12 000 IU; vitamin D3, 5000 IU; vitamin E, 30 mg; vitamin K3, 2.3 mg; vitamin B1, 1.0 mg; vitamin B2, 4.5 mg; vitamin B6, 2.7 mg; vitamin B12, 20 μg; niacine, 40 mg; d-pantothenic acid, 9 mg; choline chloride, 500 mg; folic acid, 0.5 mg; biotin, 100 μg; FeSO4.H2O, 150 mg; CuSO4.5H2O, 40 mg; MnO, 100 mg; ZnSo4.H2O, 145 mg; KJ, 2.0 mg; Na2SeO3, 0.56 mg; antioxidant (oxytrap PXN), 125 mg.

3 Supplied per kg diet: vitamin A, 10 000 IU; vitamin D3, 2000 IU; vitamin E, 20 mg; vitamin K3, 2.3 mg; vitamin B1, 0.8 mg; vitamin B2, 4.5 mg; vitamin B6, 1.9 mg; vitamin B12, 20 μg; niacine, 30 mg; D-pantothenic acid, 8 mg; choline chloride, 400 mg; folic acid, 0.5 mg; biotin, 50 μg; FeSO4.H2O, 150 mg; CuSO4.5H2O, 40 mg; MnO, 100 mg; ZnSo4.H2O, 145 mg; KJ, 1.9 mg; Na2SeO3, 0.50 mg; antioxidant (oxytrap PXN), 125 mg.

Housing and management

Hatching eggs (n=2160; weight range 58 to 69 g) of a Ross 308 breeder flock (42 weeks of age) were incubated at a temperature of 37.5°C and 54.0% relative humidity. After removal from the incubator, 576 male chickens were kept in a grow-out facility for 28 days. Female chickens were excluded from the experiment. The facility contained 96 cages (50×50 cm) with six chickens per cage. Treatments were randomly assigned to cages within 16 blocks, resulting in 16 replications per treatment. Cage floors were covered with 2 cm of wood shavings. Each cage was equipped with two nipple drinkers adjustable in height. Artificial lighting was set to 23 h/day from 0 to 2 days, 20 h/day from 2 to 6 days and 18 h/day from 6 days onwards. Temperature was set at 34°C at the start and set to decrease gradually until a final temperature of 22.1°C was reached at 18 days. Temperature was fixed at this level for the remainder of the experiment.

Growth performance

Feed intake and BW were determined at 0, 2, 7, 14, 21, 25 and 28 days during the grow-out period. Feed intake was recorded per cage, while BW was recorded individually. Gain to feed ratio was calculated based on calculated BW gain and feed intake per cage.

Immunological analysis

At 2 days (in advance of feed access for delayed fed broiler chickens), one randomly chosen chicken per cage was killed by decapitation for blood collection. From 7 days onward, one chicken per cage was selected for weekly blood sampling from the brachial vein. In addition, a sample was collected at 4 days after immunization (day 25). Blood samples were taken before switching to a new feeding phase and in advance of immunization. Serum was stored after decantation at −80°C for further analysis.

Immunoglobulins

Serum samples were analyzed to detect natural antibodies (NAb) IgM and IgY titers against Keyhole Limpet Hemocyanin (KLH) using similar methodology as described by Lammers et al. (2004). Antibody titers measured against KLH were expressed as the 2log values of the dilutions that gave an extinction closest to 50% of the highest mean extinction of a standard positive present on every microtiter plate.

Agglutination titer

Total serum antibody titers to SRBC were only determined at 21, 25 and 28 days (0, 3 and 7 days post immunization). SRBC antibody titers were assessed by agglutination according to methodology previously described by Van der Zijpp and Leenstra (1980). Antibody titers measured against SRBC were expressed as the 2log of the reciprocal of the highest serum dilution giving complete agglutination.

IFN-γ

Serum was analyzed using a commercial sandwich type ELISA kit (Chicken IFN-γ CytoSetTM; cat. no. CAC1233; Invitrogen, CA, USA) and expressed as the amount of picogram per mililiter.

Complement activity

Complement activity was not measured at day 2. Activity was measured using a hemolytic technique as described by Parmentier et al. (2002) with an adapted light-scattering method. Serum was diluted and incubated with either sensitized sheep erythrocytes (Hemolysins, ref. no. 72 202; Biomérieux, the Netherlands) to measure activity of the classical pathway (CPW) or rabbit erythrocytes to measure activity of the alternative pathway (APW). Hemolytic complement activity was scored and expressed as ‘yes’ or ‘no’ based on lysis of erythrocytes.

Statistical analysis

Data were analyzed in SAS (Version 9.3, 2011, SAS Institute Inc., Cary, NC, USA) using cage as the experimental unit. The dietary treatment period (0 to 7 days), grow-out period (7 to 21 days) and immunization period (21 to 28 days) were separately analyzed as the chicken underwent different physiological processes during these periods.

Growth performance data (BW gain, feed intake and gain to feed ratio) and immune data until 2 days were subjected to mixed model analysis using the PROC MIXED procedure. The following statistical model was used: Y ijk =μ+α i +β j +α×β ij +b k +e ijk, where Y ijk is the dependent variable, μ the overall mean, α i the fixed effect of moment of feed access (i=direct or delayed), β j the fixed effect of pre-starter composition (j=control, fish oil or MCFA), b k the random block effect (k=1, 2, 3, …, 16) and e ijk the residual error term. For data from 0 to 2 days, effects of feed access and the interaction with pre-starter composition were excluded from the model. Mortality data were analyzed as survival data to test homogeneity of survival curves, using the PROC LIFETEST procedure.

Immunological data were considered repeated measures from 7 days onwards and therefore subjected to mixed model analysis using the repeated lines statement. Hemolytic complement activity was analyzed using the PROC GLIMMIX procedure including the repeated lines statement. The three-way interaction between day, feed access and pre-starter composition did not solve and was therefore omitted from the model. Output is expressed as the chance for a complement response.

As the applied dietary treatments had only limited effects on humoral immune function, outcomes of the immunological analysis are only described in the Results section. However, a tabular overview is provided in Supplementary Tables S1 to S4 of Supplementary material S1. Although not the aim of the experiment, the current experiment also provided insight in general humoral immune responses in time (0 to 28 days) of broiler chickens. These results are described in Supplementary material S1 and presented in Supplementary Tables S1 to S4 and Supplementary Figure S1.

Data are reported as least square means and differences between treatment means are assumed to be significant when P⩽0.05.

Results

General

For mortality from 0 to 28 days, an interaction was found for feed access and pre-starter composition (P=0.014; Figure 1). Chickens with direct feed access fed the control pre-starter diet had higher risk for mortality than chickens with delayed feed access fed the control pre-starter diet (16.7% v. 4.2%).

Figure 1 Mortality rate of broiler chickens, expressed per treatment. (1) Direct feed access & control pre-starter, (2) direct feed access & fish oil pre-starter, (3) direct feed access & medium chain fatty acids (MCFA) pre-starter, (4) delayed (48 h) feed access & control pre-starter, (5) delayed (48 h) feed access & fish oil pre-starter, (6) delayed (48 h) feed access & MCFA pre-starter. Feed access effect: P=0.002, Diet effect: P=0.428. Moment of feed access x diet interaction effect: P=0.014. Cumulative mortality rates with different superscripts differ significantly at P<0.05.

Dietary treatment period (0 to 7 days)

No interaction was found between feed access and pre-starter composition for any of the performance and immune variables from 2 to 7 days. BW gain and feed intake from 2 to 7 days of direct fed chickens were 34.9% and 54.0% higher compared with delayed fed chickens (both P<0.001; Table 2). Gain to feed ratio was lower for direct fed chickens compared with delayed fed chickens (−0.149; P<0.001; Table 2).

Table 2 Effects of moment of feed access and pre-starter composition on BW, BW gain, feed intake and gain to feed ratio of broiler chickens 0 to 21 days (LSmeans) 1

FA=feed and water access; DIR=direct access; DEL=delayed access (48 h); DIET=pre-starter diet; CONT=control; FISH=fish oil; MCFA=medium chain fatty acids.

A,BValues within a row with different superscripts differ significantly at P<0.01.

1 Each cage contained six male broilers at the start of the experiment. For analysis of data collected from 0 to 2 days, effects of feed and water access and the interaction with pre-starter composition were excluded from the model.

Provision of MCFA in the pre-starter diet resulted in a higher BW gain from 2 to 7 days (4.8% on average; P=0.010), and a higher gain to feed ratio (1.132 v. 1.102 and 1.094, respectively; P=0.004) compared with the control and fish oil pre-starter diets (Table 2). Feed access and pre-starter composition did not affect KLH specific NAb levels, IFN-γ, and the complement CPW and APW response during the pre-starter period.

Grow-out period (7 to 21 days)

A tendency for interaction between feed access and pre-starter composition was found for BW gain from 7 to 21 days (P=0.097; Table 2). Within the direct fed chickens, provision of MCFA in the pre-starter diet resulted in a 1.6% lower BW gain compared with the control and fish oil containing pre-starter diets, whereas this was opposite for delayed fed chickens (3.4% higher BW gain for the MCFA pre-starter diet). BW gain and feed intake from 7 to 21 days of direct fed chickens were, respectively, 18.5% and 20.3% higher compared with delayed fed chickens (both P<0.001; Table 2). Gain to feed ratio was lower for direct fed chickens compared with delayed fed chickens (0.736 v. 0.747; P=0.005; Table 2). Starter diet composition tended to affect the alternative complement pathway response from 7 to 21 days (P=0.093), where MCFA and fish oil containing starter diets had a lower chance for an APW complement response compared with the control starter diet. Feed access and pre-starter composition did not affect KLH specific NAb levels, IFN-γ, and complement CPW response during the grow-out period.

Immunization period (21 to 28 days)

The results are reported in Tables 3 and 4. An interaction was found between feed access and pre-starter composition for BW at 28 days (P=0.033; Table 4). Within the direct fed chickens, the control pre-starter diet had the highest BW and the MCFA containing pre-starter diet the lowest (Δ=2.4%), whereas this was the opposite for the delayed fed chickens (Δ=3.0%). Furthermore, a tendency for interaction between feed access and pre-starter diet was found for feed intake between 21 and 25 days (P=0.066; Table 4). Within the direct fed chickens, the control pre-starter diet had a higher feed intake than the MCFA pre-starter diet (Δ=3.5%), whereas this was opposite in the delayed fed chickens (Δ=2.4%). BW gain between 21 and 25 days for direct fed chickens was 7.3% higher compared with delayed fed chickens (P<0.001; Table 3), but no treatment effect was found on BW gain from 25 to 28 days. Feed intake from 21 to 28 days of direct fed chickens was 8.3% higher compared with delayed fed chickens (P<0.001; Table 3). Gain to feed ratio from 21 to 25 days, as well as from 25 to 28 days, was lower for direct fed chickens compared with delayed fed chickens (P=0.001 and 0.005; Table 3).

Table 3 Effects of moment of feed access and pre-starter composition on BW, BW gain, feed intake and gain to feed ratio of broiler chickens 21 to 28 days (LSmeans) 1

FA=feed and water access; DIR=direct access; DEL=delayed access (48 h); DIET=pre-starter diet; CONT=control; FISH=fish oil; MCFA=medium chain fatty acids.

A,BValues within a row with different superscripts differ significantly at P<0.01.

1 Each cage contained six male broilers at the start of the experiment.

Table 4 Interaction effects of moment of feed access and pre-starter composition on BW, BW gain, feed intake and gain to feed ratio of broiler chickens 21 to 28 days (LSmeans) 1

FA=feed and water access; DIR=direct access; DEL=delayed access (48 h); DIET=pre-starter diet; CONT=control; FISH=fish oil; MCFA=medium chain fatty acids.

a,bValues within a row with different superscripts differ significantly at P<0.01.

1 Each cage contained six male broilers at the start of the experiment.

Direct fed chickens had higher serum IFN-γ concentrations compared with delayed fed chickens (on average 96.9 v. 80.5 pg/ml; P=0.017). Furthermore, provision of MCFA in the pre-starter diet tended to result in higher IFN-γ concentrations from 21 to 28 days compared with the control and fish oil containing pre-starter diets (98.5 v. 84.0 and 83.5 pg/ml on average from 21 to 28 days; P=0.074). Feed access and pre-starter composition did not affect KLH specific NAb levels, agglutination titers, and the complement CPW and APW response during the immunization period.

Discussion

Moment of feed access

Delayed feed access resulted in lower BW gain from 0 to 25 days compared with direct fed chickens. A lower BW gain might be explained by impaired intestinal development, which is a direct consequence of delayed feed access as demonstrated by Noy et al. (2001). Impaired intestinal development has been described by a lowered relative weight of the intestinal tract, shortened intestinal length, changed villi density, lowered villi height and a lowered number of goblet cells per villus (Maiorka et al., 2003). A too long period of feed withdrawal may cause a permanent impairment of growth from which chickens do not recover by means of compensatory growth and performance. In the current experiment, chickens were indeed not capable to recover from delayed feed access for 48 h, although differences became smaller and non-significant from 25 days onwards. In the current experiment, the partial compensatory growth was reflected by chickens with delayed feed access having a higher gain to feed ratio throughout the experimental period than those with direct feed access. An improved feed efficiency of broiler chickens from 0 to 21 days after a period of feed restriction was found not to be related to a lowered maintenance requirement nor continued lower metabolic rate as a consequence of feed restriction. However, a higher metabolizable energy intake as a result of a higher feed intake relative to body size, does improve feed efficiency (Zubair and Leeson, 1994).

In the current experiment, an interaction was found for mortality rate from 0 to 28 days between feed access and pre-starter composition, although this was primarily caused by differences between direct and delayed fed chickens that were fed the control pre-starter diet. Differences in mortality might relate to the metabolic status of the chicken during the first week after hatch. Various studies have suggested a positive relationship between restricted feeding and a lowered mortality risk due to lower occurrence of ascites (Balog, 2003; Wijtten et al., 2010). Delayed feed access after hatch can be considered as a form of feed restriction too and as such may cause a similar effect. Feed restriction has been related to a lowered metabolic rate and subequently a lower oxygen requirement, possibly resulting in less ascites associated health problems (Wijtten et al., 2010). Therefore, delayed feed access after hatch may result in a physiological benefit over direct feeding by means of a lowered mortality risk. However, in other research where chickens were delayed fed for 1 or 2 days, the mortality risk was not affected (Corless and Sell, 1999). In chickens that were infected with the malabsorption syndrome, inclusion of MCFA resulted in a lower mortality risk (Gutierrez Del Alamo et al., 2007) of which the effect was contributed to the antimicrobial properties of MCFA (Van Immerseel et al., 2004). Inclusion of MCFA in a pre-starter diet can be hypothesized to have similar antimicrobial properties, possibly preventing the colonization of pathogenic microflora associated with increased mortality risk. It remains up for discussion then why a similar effect of MCFA on mortality risk was not found in delayed fed broiler chickens and if this for example is related to the amount of feed intake or timing of feeding.

Chickens with direct feed access had higher concentrations of IFN-γ 21 to 28 days compared with chickens with delayed feed access for 48 h. IFN-γ is predominantly produced by natural killer cells as part of the innate immune response, followed by CD4+ and CD8+ T cells during the acquired immune response (Schoenborn and Wilson, 2007). This advocates that also T cells are capable of producing IFN-γ when stimulated by antigens, next to natural killer cells. Delayed feed access may result in delayed colonization of the cecum and colon by T cells, as well as expression of IL-2 mRNA in hindgut T cells (Bar-Shira et al., 2005). The latter might suggest that chickens with delayed feed access are less able to produce IFN-γ around the gastrointestinal tract compared with direct fed chickens, as T cells produce IFN-γ in response to IL-2 stimulation.

In the current experiment, delayed feed access did not strongly affect the measured parameters for humoral immune function and response after a SRBC challenge, while in other experiments the immune response was impaired when exposed to an immunological challenge in later life (Bar-Shira et al., 2005; Simon et al., 2015). This suggests that the measured immune responses that are initially related to a dietary treatment, may also strongly depend on the type of immunological challenge used.

Pre-starter composition

Inclusion of MCFA in the pre-starter diet resulted in higher BW gain and gain to feed ratio (not feed intake) compared with the control and fish oil containing pre-starter diets, but only during the period the pre-starter diet was provided (till 7 days). However, a tendency for interaction between moment of feed access and pre-starter composition was found as well for BW gain and feed intake from 7 to 25 days. It appears that a MCFA pre-starter diet is most effective for chickens with delayed feed access and it might be hypothesized that inclusion of MCFA in a pre-starter diet had a beneficial effect on the recovery of the gastrointestinal tract after an initial period of feed deprivation. MCFA are known to increase tight junction permeability of mucosal tissue (Lindmark et al., 1998). Increased tight junction permeability may impair the intestinal barrier functionality and may thus result in increased susceptibility to pathogens and a transfer of larger toxic molecules. However, the disadvantage of increased tight junction permeability seems to be outweighed in an intestine that is already damaged, because it may also result in a more rapid absorption of nutrients, such as glucose (Ballard et al., 1995). These nutrients may be required as an energy source for intestinal recovery. Besides increasing tight junction permeability of mucosal tissue, MCFA by themselves may also function as an easily accessible energy supply for enterocytes and thus cell recovery due to their relatively high digestibility coefficient at hatch compared with other fats (0.86 for polyunsaturated fatty acids v. 0.61 for soybean oil; Noy and Sklan, 1995, Turner et al., 1999, Batal and Parsons, 2002). Hence, MCFA might have a beneficial effect in the intestine of delayed fed chickens only during a restoration phase, meaning that in direct fed chickens that do not need to restore their intestinal integrity, MCFA lack this beneficial effect.

Inclusion of fish oil in the pre-starter diet did not affect natural anti-KLH IgY titers. However, Wang et al. (2000) found increased IgY levels (+30%) when feeding layer chickens from 0 to 8 weeks of age fed a diet containing 5% fish oil v. sunflower oil, animal oil blend or linseed oil. Therefore, the current inclusion level of fish oil (0.5%) may have been too low to find effects on the humoral immune system.

In summary, delayed feed access for day old chicks resulted in lower growth performance compared with direct access. Based on partial compensatory growth, it can be suggested that the current period of delayed feed access did not result in a permanent impairment of the chickens’ growth capacity. Feeding MCFA in the pre-starter diet resulted in higher BW gain and gain to feed ratio, but only during the period the diets were provided. Feeding a MCFA containing pre-starter diet tends to be most effective for delayed fed broiler chickens by means of higher growth performance, but most effective for direct fed chickens with respect to a lowered mortality risk. Current inclusion levels of fish oil and MCFA in the pre-starter diet appear to have limited (long-term) effects on growth and development, as well as on humoral immune function.

Acknowledgments

The authors gratefully acknowledge the help and assistance from the staff of the Cargill Animal Nutrition Innovation Center Velddriel (the Netherlands) and the Adaptation Physiology Group of Wageningen University (the Netherlands) during the study.

Conflicts of Interest

The authors declare that there is no conflict of interest.

Supplementary material

For supplementary material/s referred to in this article, please visit http://dx.doi.org/10.1017/S1751731116000288

References

ST Ballard , JH Hunter and AE Taylor 1995. Regulation of tight-junction permeability during nutrient absorption accross the intestinal epithelium. Annual Review of Nutrition 15, 3555. doi:10.1146/annurev.nu.15.070195.000343.
JM Balog 2003. Ascites syndrome (pulmonary hypertension syndrome) in broiler chickens: Are we seeing the light at the end of the tunnel? Avian and Poultry Biology Reviews 14, 99126.
E Bar-Shira , D Sklan and A Friedman 2005. Impaired immune responses in broiler hatchling hindgut following delayed access to feed. Veterinary Immunology and Immunopathology 105, 3345.
A Batal and C Parsons 2002. Effects of age on nutrient digestibility in chicks fed different diets. Poultry Science 81, 400407.
VL Christensen 2009. Development during the first seven days post-hatching. Avian Biology Research 2, 2733.
AB Corless and JL Sell 1999. The effects of delayed access to feed and water on the physical and functional development of the digestive system of young turkeys. Poultry Science 78, 11581169.
A Gutierrez Del Alamo , H Enting , J De Los Mozos and P Perez de Ayala 2007. The effect of dietary short and medium chain fatty acids on the performance of broiler chickens. Proceedings of the 19th Australian Poultry Science Symposium, 12 to 14 February 2007, Sydney, Australia, pp. 169–172.
DR Korver 2012. Implications of changing immune function through nutrition in poultry. Animal Feed Science and Technology 173, 5464.
DR Korver and KC Klasing 1997. Dietary fish oil alters specific and inflammatory immune responses in chicks. The Journal of Nutrition 127, 20392046.
A Lammers , MEV Klomp , MGB Nieuwland , HFJ Savelkoul and HK Parmentier 2004. Adoptive transfer of natural antibodies to non-immunized chickens affects subsequent antigen-specific humoral and cellular immune responses. Developmental and Comparative Immunology 28, 5160.
DM Lamot , IB van de Linde , R Molenaar , CW van der Pol , PJA Wijtten , B Kemp and H van den Brand 2014. Effects of moment of hatch and feed access on chicken development. Poultry Science 93, 26042614.
JY Lee , KH Sohn , SH Rhee and D Hwang 2001. Saturated fatty acids, but not unsaturated fatty acids, induce the expression of cyclooxygenase-2 mediated through toll-like receptor 4. Journal of Biological Chemistry 276, 1668316689.
T Lindmark , Y Kimura and P Artursson 1998. Absorption enhancement through intracellular regulation of tight junction permeability by medium chain fatty acids in caco-2 cells. Journal of Pharmacology and Experimental Therapeutics 284, 362369.
A Maiorka , E Santin , F Dahlke , IC Boleli , RL Furlan and M Macari 2003. Posthatching water and feed deprivation affect the gastrointestinal tract and intestinal mucosa development of broiler chicks. Journal of Applied Poultry Research 12, 483492.
Y Noy , A Geyra and D Sklan 2001. The effect of early feeding on growth and small intestinal development in the posthatch poult. Poultry Science 80, 912919.
Y Noy and D Sklan 1995. Digestion and absorption in the young chick. Poultry Science 74, 366373.
HK Parmentier , R Baelmans , MGB Nieuwland , P Dorny and F Demey 2002. Haemolytic complement activity, c3 and factor b consumption in serum from chickens divergently selected for antibody responses to sheep red blood cells. Veterinary Immunology and Immunopathology 90, 91100.
JR Schoenborn and CB Wilson 2007. Regulation of interferon-gamma during innate and adaptive immune responses. Advances in Immunology 96, 41101.
K Simon , G de Vries Reilingh , JE Bolhuis , B Kemp and A Lammers 2015. Early feeding and early life housing conditions influence the response towards a noninfectious lung challenge in broilers. Poultry Science 94, 20412048.
K Simon , G de Vries Reilingh , B Kemp and A Lammers 2014. Development of ileal cytokine and immunoglobulin expression levels in response to early feeding in broilers and layers. Poultry Science 93, 30173027.
DV Thomas , V Ravindran and G Ravindran 2008. Nutrient digestibility and energy utilisation of diets based on wheat, sorghum or maize by the newly hatched broiler chick. British Poultry Science 49, 429435.
K Turner , T Applegate and M Lilburn 1999. Effects of feeding high carbohydrate or fat diets. 2. Apparent digestibility and apparent metabolizable energy of the posthatch poult. Poultry Science 78, 15811587.
LJF Van de Ven , AV van Wagenberg , E Decuypere , B Kemp and H van den Brand 2013. Perinatal broiler physiology between hatching and chick collection in 2 hatching systems. Poultry Science 92, 10501061.
AJ Van der Zijpp and FR Leenstra 1980. Genetic analysis of the humoral immune response of white leghorn chicks. Poultry Science 59, 13631369.
F Van Immerseel , J De Buck , F Boyen , L Bohez , F Pasmans , J Volf , M Sevcik , I Rychlik , F Haesebrouck and R Ducatelle 2004. Medium-chain fatty acids decrease colonization and invasion through hila suppression shortly after infection of chickens with Salmonella enterica serovar Enteritidis. Applied and Environmental Microbiology 70, 35823587.
I Walstra 2011. Adaptive capacity of rearing hens: effects of early life conditions. PhD thesis, Wageningen University, Wageningen, The Netherlands.
YW Wang , CJ Field and JS Sim 2000. Dietary polyunsaturated fatty acids alter lymphocyte subset proportion and proliferation, serum immunoglobulin g concentration, and immune tissue development in chicks. Poultry Science 79, 17411748.
PJA Wijtten , E Hangoor , JKWM Sparla and MWA Verstegen 2010. Dietary amino acid levels and feed restriction affect small intestinal development, mortality, and weight gain of male broilers. Poultry Science 89, 14241439.
AK Zubair and S Leeson 1994. Effect of early feed restriction and realimentation on heat production and changes in sizes of digestive organs of male broilers. Poultry Science 73, 529538.