We conducted a study to evaluate the effects of intramuscular fat levels on the sensory characteristics of duck breast meat. Combining duck genotypes (Muscovy, Pekin, and their crossbreed hinny and mule ducks) and feeding levels (overfeeding between 12 and 14 wk of age vs. ad libitum feeding) enabled us to obtain a wide range of lipid levels in breast muscle. The average values were between 2.55 and 6.40 g per 100 g of muscle. Breast muscle from overfed ducks showed higher lipid and lower water levels than breast muscle from ducks fed ad libitum. Muscle from the overfed ducks was also paler in color and exhibited greater yellowness and cooking loss values. Juiciness was judged lower and flavor more pronounced in overfed ducks. Muscovy ducks exhibited higher breast weight and lower lipid levels than the other genotypes. At the other extreme, Pekin ducks exhibited the highest lipid levels and the lowest breast weights; values for these criteria were intermediate in hinny and mule ducks. Breast muscle of Muscovy ducks was paler, less red, and more yellow than that of other genotypes. Breast muscle of Pekin ducks exhibited the lowest values for lightness, yellowness, and energy necessary to shear meat, as well as the highest cooking loss values, and was judged more tender, juicy and less stringy than that of other genotypes. In contrast, scores for breast muscle of Muscovy ducks were the lowest for tenderness, juiciness, and flavor, and the highest for stringiness. Breast muscle of hinny and mule ducks scored the highest values for redness. Hinny ducks also scored the highest values for flavor. Genotype exerted a higher effect on the sensory quality of breast muscle than did feeding levels. Finally, increasing lipid levels in breast muscle increased lightness, yellowness, cooking loss, tenderness, and flavor, with correlation coefficients of 0.49, 0.47, 0.54, 0.43, and 0.28, respectively. However, breast meat color and tenderness were mainly influenced by genotype.

To investigate the effect of overfeeding on the ileal and cecal microbiota of two genotypes of ducks (Pekin and Muscovy), high-throughput 16S rRNA gene-based pyrosequencing was used. The ducks were overfed for 12 days with 58% maize flour and 42% maize grain. Samples were collected before the overfeeding period (at 12 weeks), at 13 weeks, at 14 weeks, and 3 h after feeding. In parallel, ducks fed ad libitum were killed at the same ages. Whatever the digestive segment, the genotype, and the level of intake, Firmicutes and Bacteroidetes are the dominant phyla in the bacterial community of ducks (at least 80%). Before overfeeding, ileal samples were dominated by Bacilli, Clostridia, and Bacteroidia classes (≥ 70%), and cecal samples, by Bacteroidia and Clostridia classes (around 90%) in both Pekin and Muscovy ducks. The richness and diversity decreased in the ileum and increased in the ceca after overfeeding. Overfeeding triggers major changes in the ileum, whereas the ceca are less affected. Overfeeding increased the relative abundance of Clostridiaceae, Lactobacillaceae, Streptococcaceae, and Enterococcaceae families in the ileum, whereas genotype affects particularly three families: Lachnospiraceae, Bacteroidaceae, and Desulfovibrionaceae in the ceca.

Since anterior pituitary expresses prolactin receptors, prolactin secreted by lactotropes could exert autocrine or paracrine actions on anterior pituitary cells. In fact, it has been observed that prolactin inhibits its own expression by lactotropes. Our hypothesis is that prolactin participates in the control of anterior pituitary cell turnover. In the present study, we explored the action of prolactin on proliferation and apoptosis of anterior pituitary cells and its effect on the expression of the prolactin receptor. To determine the activity of endogenous prolactin, we evaluated the effect of the competitive prolactin receptor antagonist Δ1-9-G129R-hPRL in vivo, using transgenic mice that constitutively and systemically express this antagonist. The weight of the pituitary gland and the anterior pituitary proliferation index, determined by BrdU incorporation, were higher in transgenic mice expressing the antagonist than in wild-type littermates. In addition, blockade of prolactin receptor in vitro by Δ1-9-G129R-hPRL increased proliferation and inhibited apoptosis of somatolactotrope GH3 cells and of primary cultures of male rat anterior pituitary cells, including lactotropes. These results suggest that prolactin acts as an autocrine/paracrine antiproliferative and proapoptotic factor in the anterior pituitary gland. In addition, anterior pituitary expression of the long isoform of the prolactin receptor, measured by real-time PCR, increased about 10-fold in transgenic mice expressing the prolactin receptor antagonist, whereas only a modest increase in the S3 short-isoform expression was observed. These results suggest that endogenous prolactin may regulate its own biological actions in the anterior pituitary by inhibiting the expression of the long isoform of the prolactin receptor. In conclusion, our observations suggest that prolactin is involved in the maintenance of physiological cell renewal in the anterior pituitary. Alterations in this physiological role of prolactin could contribute to pituitary tumor development.

Anterior pituitary cell turnover occurring during female sexual cycle is a poorly understood process that involves complex regulation of cell proliferation and apoptosis by multiple hormones. In rats, the prolactin (PRL) surge that occurs at proestrus coincides with the highest apoptotic rate. Since anterior pituitary cells express the prolactin receptor (PRLR), we aimed to address the actual role of PRL in the regulation of pituitary cell turnover in cycling females. We showed that acute hyperprolactinemia induced in ovariectomized rats using PRL injection or dopamine antagonist treatment rapidly increased apoptosis and decreased proliferation specifically of PRL producing cells (lactotropes), suggesting a direct regulation of these cell responses by PRL. To demonstrate that apoptosis naturally occurring at proestrus was regulated by transient elevation of endogenous PRL levels, we used PRLR-deficient female mice (PRLRKO) in which PRL signaling is totally abolished. According to our hypothesis, no increase in lactotrope apoptotic rate was observed at proestrus, which likely contributes to pituitary tumorigenesis observed in these animals. To decipher the molecular mechanisms underlying PRL effects, we explored the isoform-specific pattern of PRLR expression in cycling wild type females. This analysis revealed dramatic changes of long versus short PRLR ratio during the estrous cycle, which is particularly relevant since these isoforms exhibit distinct signaling properties. This pattern was markedly altered in a model of chronic PRLR signaling blockade involving transgenic mice expressing a pure PRLR antagonist (TGΔ1–9-G129R-hPRL), providing evidence that PRL regulates the expression of its own receptor in an isoform-specific manner. Taken together, these results demonstrate that i) the PRL surge occurring during proestrus is a major proapoptotic signal for lactotropes, and ii) partial or total deficiencies in PRLR signaling in the anterior pituitary may result in pituitary hyperplasia and eventual prolactinoma development, as observed in TGΔ1–9-G129R-hPRL and PRLRKO mice, respectively.