Animal growth is a complex and dynamic process that involves physiological and morphological changes from hatching to maturity. It is defined as the increase in body size per time unit. Mathematical functions, called growth models, have been used to explain growth patterns. The aim of this study was to compare the Gompertz-Laird, logistic, Richards, and Von Bertalanffy growth models to determine which best fits the data of the Creole chickens ( CC ). Three hundred forty-seven CC were individually weighed from hatching until 177 D of age. Birds were fed a starter diet (0–18 D of age; 19% crude protein ( CP ) and 3,000 kcal of ME/kg) and grower diet (19–177 D of age; 18% CP and 2,800 kcal of ME/kg). Data were analyzed using PROC NLIN to fit the nonlinear growth curve. The coefficient of determination ( R 2 ), Akaike information criteria ( AIC ), and Bayesian information criteria ( BIC ) were used to compare the goodness of fit of the models. The Von Bertalanffy (R 2 : 0.9382, 0.9415; AIC: 2,224.1, 2,424.8; BIC: 2,233.5, 2,434.3, for females and males, respectively) was the model that best explained growth of the birds. On the other hand, both the Gompertz-Laird and logistic models overestimated hatching BW and underestimated the final BW of CC. Females reached age of maximum growth faster than males. The asymptotic weight was higher in males (3,011 g) than in females (2,011 g). Body weight at inflection point was 892 g at 64 D of age for males and 596 g at 54 D for females. In conclusion, the best fit of the data was obtained with the Von Bertalanffy growth model; the information is intended to serve as the basis for utilizing CC.

We report the genetic relationship between growth and bone quality traits in a random mating broiler control population. Traits studied were growth rates from week 0 to 4 [body weight gain (BWG) 0 to 4], from week 0 to 6 (BWG 0 to 6), and residual feed intake (RFI) from week 5 to 6 (RFI 5 to 6). Bone quality traits were obtained at 6 weeks of age. These traits were shank weight (SW), shank length (SL), shank diameter (SDIAM), tibia weight (TW), tibia length (TL), and tibia diameter (TDIAM). Likewise, tibia was used to obtain the tibia density (TDEN), tibia breaking strength (TBS), tibia mineral density (TMD), tibia mineral content (TMC), and tibia ash content (TAC). At the phenotypic level, growth traits were positively correlated with most of the bone quality traits except with TDEN and TAC which tended to show unfavorable associations (-0.04 to -0.31). Heritability of bone quality traits ranged from 0.08 to 0.54. The additive genetic associations of growth traits with weight, length, and diameter of shank and tibia were positive (0.37 to 0.80). A similar pattern was observed with TMD and TMC (0.06 to 0.65). In contrast, growth traits showed unfavorable genetic associations with TDEN, TBS, and TAC (-0.03 to -0.18). It was concluded that bone quality traits have an additive genetic background and they can be improved by means of genetic tools. It appears that selection for growth is negatively correlated with some traits involved in the integrity, health, and maturity of leg bones.

Improvement in growth has been widely reported as the cause of increased incidence of leg problems in broiler chickens. We report herein the genetic relationship between growth and leg problems in a random mating broiler control population. The traits studied were valgus (VL), varus (VR), and tibial dyschondroplasia (TD), which were expressed on a binary scale of 0 (normal) and 1 (abnormal); growth rates from 0 to 4 wk (BWG 0-4) and from 0 to 6 wk of age (BWG 0-6); and residual feed intake from 5 to 6 wk of age (RFI 5-6). A threshold-linear mixed model was employed for the joint analysis of the categorical and linear traits. Incidences of VL, VR, and TD were 26, 4, and 2%, respectively. Heritability of leg problems ranged from 0.11 to 0.13. Phenotypic correlations alluded to an unfavorable relationship between growth and leg problems; however, the genetic relationship between growth and leg problems was extremely weak, ranging from 0.01 to 0.08. There is, therefore, a basis for genetic improvement in leg problems. However, improved management practices would also be important to reduce incidence of leg problems in broiler chickens.

SummaryThis study examined the molecular mechanisms of methionine pathways in meat-type chickens where birds were provided with a diet deficient in methionine from 3 to 5 weeks of age. The birds on the deficient diet were then provided with a diet supplemented with either D,L-methionine or D,L-HMTBA from 5 to 7 weeks. The diet of the control birds was supplemented with L-methionine from hatch till 7 weeks of age.We studied the mRNA expression of methionine adenosyltransferase 1, alpha, methionine adenosyltransferase 1, beta, 5-methyltetrahydrofolate-homocysteine methyltransferase, 5-methyltetrahydrofolate-homocysteine methyltransferase reductase, betaine-homocysteine S-methyltransferase, glycine N-methyltransferase, S-adenosyl-L-homocysteine hydrolase and cystathionine beta synthase genes in the liver, duodenum, Pectoralis (P.) major and the gastrocnemius muscle at 5 and 7 weeks. Feeding a diet deficient in dietary methionine affected body composition. Birds that were fed a methionine-deficient diet expressed genes that indicated that remethylation occurred via the one-carbon pathway in the liver and duodenum; however, in the P. major and the gastrocnemius muscles, gene expression levels suggested that homocysteine received methyl from both folate and betaine for remethylation. Birds who were switched from a methionine deficiency diet to one supplemented with either D,Lmethionine or D,L-HMTBA showed a downregulation of all the genes studied in the liver. However, depending on the tissue or methionine form, either folate or betaine was elicited for remethylation. Thus, mRNA expressions show that genes in the remethylation and transsulphuration pathways were regulated according to tissue need, and there were some differences in the methionine form.

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