Genetic selection has significantly improved the muscle development of fast-growing broiler chickens in the last 50 yr. However, improvement in muscle growth has coincided with relatively poor development of visceral systems, resulting in impaired ability to cope with high environmental temperatures. The aim of this study was to elucidate the effects of thermal manipulation (TM) during different periods of embryogenesis on chick hatchability, BW and thermoregulation upon hatching, on their ability to cope with thermal challenge at 42 d of age, and on carcass and breast meat traits. Control embryos were incubated at 37.8 degrees C. The TM embryos were incubated at 37.8 degrees C and treated for 3 h at 39.5 degrees C on the following days of embryogenesis: E8 to E10 [early (EA)], E16 to E18 [late (LA)], and both E8 to E10 and E16 to E18 (EA-LA). Body weight and body temperature (T(b)) were measured at hatching and throughout the growth period as well as during exposure of 42-d-old chickens to a thermal challenge at 35 degrees C for 6 h. The LA and EA chicks exhibited significantly lower T(b) than control chicks (37.9 vs. 38.2 degrees C) at hatching, but during the growth period, differences in T(b) between treated and control chicks decreased with age. Significant hyperthermia (over 44 degrees C) was monitored in all groups during the thermal challenge, but mortality was higher in treated than in control chickens. No effect of treatments on BW was found during the entire growth period. However, breast yield was higher in LA chickens than in controls at slaughter. The EA and EA-LA treatments slightly decreased the ultimate pH of breast meat, whereas the LA treatment had no effect. In conclusion, none of the TM conditions tested in the present study were able to improve long-term thermotolerance in chickens. Late treatment favored breast muscle growth without affecting ultimate pH and drip loss of breast meat.

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In order to evaluate the role of insulin in chicken, an insulin immuno-neutralization was performed. Fed chickens received 1 or 3 i.v. injections of anti-insulin serum (2-h intervals), while fed or fasted controls received normal serum. Measurements included insulin signaling cascade (at 1 h in liver and muscle), metabolic or endocrine plasma parameters (at 1 and 5 h), and qRT-PCR analysis (at 5 h) of 23 genes involved in endocrine regulation, metabolisms, and transcription. Most plasma parameters and food intake were altered by insulin privation as early as 1 h and largely at 5 h. The initial steps of insulin signaling pathways including insulin receptor (IR), IR substrate-1 (IRS-1), and Src homology collagen and downstream elements: phosphatidylinositol 3-kinase (PI3K), Akt, GSK3, ERK2, and S6 ribosomal protein) were accordingly turned off in the liver. In the muscle, IR, IRS-1 tyrosine phosphorylation, and PI3K activity remained unchanged, whereas several subsequent steps were altered by insulin privation. In both tissues, AMPK was not altered. In the liver, insulin privation decreased Egr1, PPARg, SREBP1, THRSPa (spot14), D2-deiodinase, glucokinase (GK), and fatty acid synthase (whereas D3-deiodinase and IGF-binding protein1 transcripts were up-regulated. Liver SREBP1 and GK and plasma IGFBP1 proteins were accordingly downand up-regulated. In the muscle, PPARbd and atrogin-1 mRNA increased and Egr1 mRNA decreased. Changes in messengers were partly mimicked by fasting. Thus, insulin signaling in muscle is peculiar in chicken and is strictly dependent on insulin in fed status. The 'diabetic' status induced by insulin immuno-neutralization is accompanied by impairments of glucagon secretion, thyroid axis, and expression of several genes involved in regulatory pathways or metabolisms, evidencing pleiotropic effects of insulin in fed chicken.