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      Post-photostimulation energy intake accelerated pubertal development in broiler breeder pullets

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          The effect of ME intake ( MEI) on the reproductive system was evaluated. Ross 308 broiler breeder pullets (n = 140) were assigned to 2 treatments from 22 to 26 wk of age: (1) Low-energy diet fed restricted (2,807 kcal/kg, low MEI) and (2) high-energy diet fed unrestricted (3,109 kcal/kg, high MEI). Daylength was increased from 8 to 14 h at 22 wk of age with a light intensity of 30 lux. Daily palpation was used to detect sexual maturity via the presence of a hard-shelled egg in the shell gland. Expression of gonadotropin releasing hormone-I ( GnRH ) and gonadotropin inhibitory hormone ( GnIH ) genes in the hypothalamus and GnRH receptor ( GnRH-RI ) and GnIH receptor ( GnIH-R ) genes in the anterior pituitary gland of each pullet was evaluated from 22 to 26 wk of age using quantitative real time-PCR. Blood samples were taken weekly and luteinizing hormone ( LH), follicle stimulating-hormone ( FSH), and 17-beta-estradiol ( E2) determined using commercial ELISA kits. Carcass samples were used for determination of CP and fat content. Data were analyzed using the MIXED procedure in SAS, and differences were reported where P ≤ 0.05. High MEI treatment pullets had 2.3-fold higher GnRH and 1.8-fold higher GnRH-RI mRNA levels than low MEI pullets. MEI affected neither expression of GnIH and GnIH-R nor carcass protein content. For high MEI (489 kcal/D) and low MEI treatments (258 kcal/D), respectively, from 22 to 26 wk of age ( P ≤ 0.05), LH concentration was 3.05 and 1.60 ng/mL; FSH concentration was 145 and 89.3 pg/mL; E2 concentration was 429 and 266 pg/mL, and carcass lipid was 13.9 and 10.3%. The onset of lay for pullets in the high MEI treatment advanced such that 100% had laid by 26 wk of age compared with 30% in the low MEI treatment. We concluded that higher MEI advanced the activation of the hypothalamic–pituitary–gonadal axis and also increased body lipid deposition, and moreover, stimulated reproductive hormone levels which overall accelerated puberty in broiler breeder pullets.

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          Most cited references 65

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            Normalization of real-time quantitative reverse transcription-PCR data: a model-based variance estimation approach to identify genes suited for normalization, applied to bladder and colon cancer data sets.

            Accurate normalization is an absolute prerequisite for correct measurement of gene expression. For quantitative real-time reverse transcription-PCR (RT-PCR), the most commonly used normalization strategy involves standardization to a single constitutively expressed control gene. However, in recent years, it has become clear that no single gene is constitutively expressed in all cell types and under all experimental conditions, implying that the expression stability of the intended control gene has to be verified before each experiment. We outline a novel, innovative, and robust strategy to identify stably expressed genes among a set of candidate normalization genes. The strategy is rooted in a mathematical model of gene expression that enables estimation not only of the overall variation of the candidate normalization genes but also of the variation between sample subgroups of the sample set. Notably, the strategy provides a direct measure for the estimated expression variation, enabling the user to evaluate the systematic error introduced when using the gene. In a side-by-side comparison with a previously published strategy, our model-based approach performed in a more robust manner and showed less sensitivity toward coregulation of the candidate normalization genes. We used the model-based strategy to identify genes suited to normalize quantitative RT-PCR data from colon cancer and bladder cancer. These genes are UBC, GAPD, and TPT1 for the colon and HSPCB, TEGT, and ATP5B for the bladder. The presented strategy can be applied to evaluate the suitability of any normalization gene candidate in any kind of experimental design and should allow more reliable normalization of RT-PCR data.
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              AMP-activated protein kinase (AMPK) is the downstream component of a protein kinase cascade that acts as an intracellular energy sensor maintaining the energy balance within the cell. This pivotal role of AMPK places it in an ideal position for regulating whole-body energy metabolism, and AMPK might play a part in protecting the body from metabolic diseases such as type 2 diabetes and obesity. Mutations in AMPK cause cardiac hypertrophy and arrhythmia. Recent findings have identified LKB1--a protein kinase that is mutated in a hereditary form of cancer--as a candidate for the upstream kinase in the AMPK cascade. AMPK could provide a link in human diseases of which the underlying cause is due to defects in energy metabolism.

                Author and article information

                Poult Sci
                Poult Sci
                Poultry Science
                28 February 2020
                April 2020
                28 February 2020
                : 99
                : 4
                : 2215-2229
                []Department of Agricultural, Food and Nutritional Science, 410 Agriculture/Forestry Centre, University of Alberta, Edmonton, AB, Canada, T6G 2P5
                []Agriculture and Agri-Food Canada, Edmonton, AB, Canada
                []Department of Animal Biosciences, University of Guelph, Guelph, ON, Canada
                Author notes
                [1 ]Corresponding author: mzuidhof@ 123456ualberta.ca

                Current address: Trouw Nutrition, Sherwood Park, AB, Canada

                © 2020 Published by Elsevier Inc. on behalf of Poultry Science Association Inc.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                Physiology and Reproduction


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