Effect of macronutrient ratio of the pre-starter diet on broiler performance and intermediary metabolism.

The aim of this study was to investigate the influence of isoenergetic substitution between the three energy delivering macronutrients in pre-starter diets on performance and intermediary nutrient metabolism in broiler chickens. From hatch until 5 days of age, 600 chicks, collected during peak of hatch, were fed one of the three experimental pre-starter diets with isoenergetic (13 MJ metabolisable energy/kg) substitutions between fat (43 vs. 108 g/kg), protein (126 vs. 240 g/kg) and carbohydrates (391 vs. 510 g/kg). After 5 days, commercial grower and finisher diets were provided. Pre-starter composition influenced body weight until slaughter age, although not statistically verifiable. Broilers fed the low protein (LP) pre-starter had the lowest body weight in relation to chickens on the low carbohydrate or low fat pre-starter diet. After hatch, chicks on the LP pre-starter diet were able to use the residual yolk sac more rapidly to fulfil their protein requirement, which is reflected in small intestine and liver development. Also, plasma metabolite levels were influenced mostly by the LP pre-starter, indicating that the main focus for the requirements of newly hatched chicks should be on proteins. Furthermore, optimal nutrition during the first day's post-hatch should take into account the contribution of the yolk.

The effects of the spread of hatch and interaction with delayed feed access after hatch on broiler performance until seven days of age.

Delay in access to feed for 1-d-old chicks impairs posthatch growth. It is a standard practice that 1-d-old chicks are deprived of feed for about 48 h before they are placed on farms. During incubation, there is a spread of 24 to 48 h for late versus early hatching. As spread of hatch increases, number of chicks that are feed-deprived for a longer time before free access (IA) to feed and water increases. In this current study, we investigated the effects of time delay in feed access on chick juvenile relative growth (RG: a measure of speed of growth) up to d 7, taking into consideration the duration of egg storage and spread of hatch. Our results confirmed that delay in feed access caused weight loss during holding time and depressed growth rate after access to feed. The magnitude of the effect depended on the hatching period within the hatching window. It also depended on whether the biological age (BA) or the chronological age (CA) of the chick was considered. Immediate access to feed produced significantly different results depending on CA or BA. Both ways, the method seemed to benefit the late hatchers. This finding contrasts with the effect of delayed feeding in which early hatchers benefited more. Long duration of egg storage depressed RG not only of chicks with immediate access to feed but also in those denied access after hatch. Delay in feed access significantly aggravated the effects of long egg storage duration on RG. Triiodothyronine levels were lower in feed-deprived chicks, and the effect was greater in late hatchers. It is concluded that the beginning of delay in feed access should be determined from the time of hatch not at the end of hatch. It is suggested that the adverse effects of delay in feed access can be reduced by providing a source of energy in hatching baskets or during transportation.

Performance and physiological parameters of broiler chickens subjected to fasting on the neonatal period.

Broiler chicks aged 12 h after hatching were allotted according to a block design in a 7 x 2 factorial schedule of 14 treatments and four replications of 50 chicks each one. The main experimental factors were fasting for 0, 6, 12, 18, 24, 30, and 36 h after chick placement and sex. Independent of sex, fasting had a negative linear effect on weight and productivity of broilers at market age (42 d) without affecting feed conversion or mortality index. Groups subjected to 18 and 36 h of fasting after placement, corresponding to 30 and 48 h posthatching fasting, had lower biometrical values for small intestine (length, weight, and size; villus height; and crypt depth) than chicks fed immediately after placement. According to the Pearson test, BW of birds at 21 and 42 d were significantly correlated to BW at 7 d (r=0.77) and 21 d (r=0.45), respectively. Males performed better than females but had higher mortality rates. Fasting did not influence serum concentrations of corticosterone or sexual steroid hormones. Nevertheless, early signs of sexual dimorphism arose from the high estradiol (E2) concentration on female serum. Heterophil:lymphocyte ratio was not different among treatments, indicating that early fasting did not seem to be a stress factor 21 or 42 d after fasting. The results suggested a maximum fasting of 24 h after hatching in order to preserve broiler productivity at market age.

Effects of storage time on incubating egg gas pressure, thyroid hormones, and corticosterone levels in embryos and on their hatching parameters.

Incubating eggs (1,800 total) produced by a commercial flock of Cobb broiler breeders were used to determine the effects of storage duration (3 and 18 d) on gas partial pressure, thyroid hormones, and hatching parameters. Partial pressure of oxygen (pO2) and carbon dioxide (pCO2) were measured on d 18 and at internal pipping (IP) during incubation. Blood samples were collected for determination of triiodothyronine (T3), thyroxine (T4), and corticosterone concentrations in the embryos at IP and in newly hatched chicks. From 464 to 510 h of incubation, eggs were checked individually every 2 h to determine the timing and duration of IP, external pipping (EP), and total hatching time. At 18 d of incubation and at IP, pCO2 was greater in air cell of eggs stored for 3 d compared to those stored for 18 d (P < 0.05), but pO2 was greater in eggs stored for 18 d. At IP, T3 and corticosterone levels were higher in plasma of the embryos of eggs stored for 3 d compared to those stored for 18 d, but it was the reverse in newly hatched chicks (P < 0.05). Embryos from eggs stored for 18 d required more time to complete IP compared to embryos of eggs stored for only 3 d (P < 0.05), whereas the duration of EP was not affected by storage. The overall longer incubation was, however, not only due to prolonged IP but also to later occurrence of IP. It was concluded that prolonged IP as a result of long storage may be related to the late increase in corticosterone level, which may be a necessary stimulus for higher T3/T4 ratio, late increase in pCO2 level, and decrease in pO2. The effect of long storage was a delay in hatching and a continuous increase in T3 due to higher corticosterone levels between IP and hatching, which may be an indication of the more stressful event of hatching of embryos from eggs stored longer. Differences in pCO2, pO2, T3, T4, and corticosterone levels in the incubating eggs may be manifestations of these changes culminating in altered hatching parameters and consequently differences in chick quality and growth potentials.

Regulation of growth hormone expression by thyrotropin-releasing hormone through the pituitary-specific transcription factor Pit-1 in chicken pituitary.

Pit-1 is a pituitary-specific POU-domain DNA binding factor, which binds to and trans-activates promoters of growth hormone- (GH), prolactin- (PRL) and thyroid stimulating hormone beta- (TSHbeta) encoding genes. Pit-1 has been identified in several mammalian and avian species. Thyrotropin-releasing hormone (TRH) is located in the hypothalamus and it stimulates TSH, GH and PRL release from the pituitary gland. In the present study, we successfully developed a competitive RT-PCR for the detection of Pit-1 expression in the chicken pituitary, that was sensitive enough to detect picogram levels of Pit-1 mRNA. Applying this method, the effect of TRH injections on Pit-1 mRNA expression was determined in the pituitary of chick embryos and growing chicks. In both 18-day-old embryos and 10-day-old male chicks the Pit-1 mRNA expression was significantly increased following TRH injection, thereby indicating that the stimulatory effects of TRH on several pituitary hormones is mediated via its effect on Pit-1 expression. Therefore, a semi-quantitative RT-PCR method was used to detect possible changes in GH levels. TRH affected the GH mRNA levels at both developmental stages. These results, combined with the data on Pit-1 mRNA expression, indicate that Pit-1 has a role in mediating the stimulatory effects of TRH on pituitary hormones like GH.