Dynamic changes of blood glucose, serum biochemical parameters and gene expression in response to exogenous insulin in Arbor Acres broilers and Silky fowls.

Silky chicken is a breed of chickens with black skin and slow growth rate used in Chinese traditional medicine, whereas Arbor Acres broiler is a well-known commercial breed in the poultry industry, it is featured by a large size, rapid-growth rate, high feed-conversion rate and strong adaptability. The difference in their rate of growth may be primarily related to different mechanism for glucose metabolism. Here we compared the insulin sensitivity of the two breeds; we investigated the temporal changes (at 0 min, 120 min and 240 min) of serum insulin and other biochemical parameters and determined the spatio-temporal changes of gene mRNA abundance in response to exogenous insulin (80 μg/kg body weight).

Single nucleotide polymorphisms in chicken lmbr1 gene were associated with chicken growth and carcass traits.

Lmbr1 is the key candidate gene controlling vertebrate limb development, but its effects on animal growth and carcass traits have never been reported. In this experiment, lmbr1 was taken as the candidate gene affecting chicken growth and carcass traits. T/C and G/A mutations located in exon 16 and one A/C mutation located in intron 5 of chicken lmbr1 were detected from Silky, White Plymouth Rock broilers and their F2 crossing chickens by PCR-SSCP and sequencing methods.

Single nucleotide polymorphisms in the chicken Lmbr1 gene are associated with chicken polydactyly.

Polydactyly is a common malformation of vertebrate limbs. Preaxial polydactyly (PPD) has been mapped in human, mouse and chicken to the syntenic region of human 7q36. Lmbr1 was thought as the critical candidate gene for human and mouse PPD.

[Progress on polydactyly character of vertebrate].

Polydactyly is a common abnormal limb phenotype in vertebrate and there is similar limb phenotype among different species. Research shows that polydactyly has a similar development mechanism, and this kind of polydactyly character seems to be controlled by homologous genes among species. The latest research results on human and mouse further shows that PPD should be caused by the disruption of a long range cis-acting regulator for Shh within Lmbr1 intron.