The study's main objective was to investigate the effects of a specifi c blend of herbal extracts (HEs) on growth performance, antioxidant status, and components of the insulin-like growth factor (IGF) system in fi nishing pigs. A total of 16 PIC (Pig Improvement Company) pigs (60.1 ± 1.2 kg; eight gilts and eight barrows) were randomly assigned to one of the two dietary groups, with four pens/group (per pen: one gilt, one barrow). The pigs were fed with a basal diet containing 0 (control) or 250 mg HEs /kg diet for 47 days. The results indicated that herbal extract supplementation led to an increase (P<0.05) on the average daily gain and serum IGF-I level, and a decrease (P<0.05) on serum malondialdehyde and feed conversion ratio. However, feed intake was not affected (P>0.05). IGF-I, insulin receptor mRNA levels (liver, stomach, duodenum, muscle) and IGF-I receptor (IGF-IR) mRNA (stomach, duodenum, muscle) were high (P<0.05), while the level of IGF-IR mRNA was low (P<0.05) in the liver tissue compared with the control pigs. The results suggest that herbal extract supplementation has an antioxidant capacity, enhance the growth performance and exhibits tissue-specifi c regulation of IGF-IR mRNA level. In addition, the results also suggest the possible physiological role of the IGF system in controlling the HEs-supported growth of fi nishing pigs.

ABSTRACT:The effects of yeast-derived protein (YP) on growth performance, intestinal health, and oxidative status of weanling piglets were investigated. A total of 80 weaned piglets (PIC 327 × 1050, 26 ± 2 days old, 6.20 ± 0.10 kg) were randomly allocated into 2 groups, 5 pens per each group and 8 piglets per each pen, receiving control diet and diet with inclusion of 4% YP at the expenses of fish meal (YP diet) for a period of 28 days. The diets were formulated to contain similar nutrient levels. Compared with control, piglets fed YP diet had markedly higher overall average daily growth (+14%, P < 0.05) and lower final feed conversion ratio (−8%, P < 0.01). Concentrations of serum serine, cystathionine, histidine, hydroxyproline, and urea were decreased in piglets fed YP diet (P < 0.05), whereas alanine and aspartate were increased (P < 0.01). Moreover, serum antioxidant enzyme activity (glutathione peroxidase) was markedly increased (+19%, P < 0.01) in piglets fed YP diet relative to piglets fed control diet. In addition, feeding YP diet considerably (P < 0.05) increased the copy numbers of lactobacilli and total bacteria in the colon of piglets at the end of the experiment. Furthermore, the mRNA abundance of innate immunity-related genes (TLR4, NF-κB1, and IL-6) was increased (P < 0.06) in the ileum of piglets fed YP diet. Collectively, results of this study indicated that diet with the inclusion of YP improved growth performance and partially enhanced anti-oxidative capability as well as intestinal innate immunity of weaning piglets.

Scope: Royal jelly (RJ) has a wide range of biological functions, its effect on hyperplasia of the mammary gland (HMG) in mammals is unclear. This study aims to investigate the effect of RJ on HMG and the dose-response relationship of RJ in the treatment of HMG. Methods and Results: HMG rats are induced by intramuscular injection of estrogen (E2) and progesterone, and are treated with different doses of RJ (100, 200, 400, and 800 mg kg -1 d -1 ). As a result, RJ improves the expansion of acinar and breast tissue ducts, particularly at 100 and 800 mg kg -1 d -1 . These two doses also inhibit serum E2 and prolactin (PRL) secretion and increase serum progesterone secretion and the expression of estrogen receptor (ER)-𝜷 in the breast tissue. In addition, 800 mg kg -1 d -1 decrease and increase the mRNA expression of, respectively, hypothalamic gonadotropin-releasing hormone (GnRH) and pituitary GnRH receptors (GnRH-R). The lowest dosage (100 mg kg -1 d -1 ) increases GnRH-R mRNA expression as well. However, the effects of 200 and 400 mg kg -1 d -1 RJ on the reproductive parameters of HMG are not significant, implying a dose-dependent effect. Conclusion: RJ regulates endocrine dyscrasia in HMG rats and improves the breast tissue structure, indicating its potential in the prevention and treatment on HMG.

Background: The ovarian hormones estrogen and progesterone profoundly influence breast cancer risk, underpinning the benefit of endocrine therapies in the treatment of breast cancer. Modulation of their effects through ovarian ablation or chemoprevention strategies also significantly decreases breast cancer incidence. Conversely, there is an increased risk of breast cancer associated with pregnancy in the short-term. The cellular mechanisms underlying these observations, however, are poorly defined. We and others recently isolated mammary epithelial populations enriched for mammary stem cells (MaSCs), committed luminal progenitor and mature luminal cells from both mouse and human mammary glands. Unexpectedly, MaSCs exhibited a receptor-negative phenotype for ERα , PR and ErbB2. Given the central important of estrogen and progesterone signaling to mammary gland development and cancer, we sought to determine whether these hormones could indirectly modulate MaSC function. Methods and Results: We utilized mouse models to directly study the effects of steroid hormones on the in vivo repopulating ability of MaSCs. Ovariectomy markedly diminished MaSC number and the extent of ductal outgrowth in vivo. The relative contribution of estrogen and progesterone to the regulation of MaSC activity was next examined using hormone pellets or antagonists. MaSC activity increased in animals treated with both estrogen and progesterone. Remarkably, even three weeks of treatment with the aromatase inhibitor letrozole was sufficient to reduce the MaSC pool. The outgrowth potential of these cells was again affected, suggesting that MaSCs retain a ‘memory’ of estrogen deprivation, perhaps through perturbation of their cycling status. Indeed, cell cycle analysis revealed an increase in the percentage of MaSC-enriched cells in G0/G1 in ovariectomized glands compared to controls. This was accompanied by a profound reduction in the expression of cell cycle genes including Cyclin D1. We further evaluated the effect of the hormonal environment on MaSC function during pregnancy, where progesterone (and prolactin) have prominent roles. Pregnancy led to a transient 11-fold increase in MaSC numbers. This was accompanied by marked elevation in the expression of the progesterone target gene RANK ligand in luminal cells, together with its receptor RANK in the MaSC-containing population. To determine whether MaSC activity is in part mediated through paracrine signals from RANK ligand, inhibitors of RANK signaling were evaluated. Treatment of virgin or pregnant mice with an anti-RANK ligand monoclonal antibody in vivo significantly impaired the clonogenic activity of the MaSC-enriched but not luminal subpopulation. Discussion: Despite lacking the steroid hormone receptors ERα and PR, MaSCs appear to be exquisitely sensitive to hormone signaling, presumably via paracrine signaling that includes the RANK signaling pathway. The augmented MaSC pool during pregnancy suggests a cellular basis for the short-term increase in breast cancer incidence following pregnancy. Our findings further indicate that breast cancer chemoprevention may in part be achieved through suppression of MaSC function. We speculate that inhibitors of RANK and other stem cell signaling pathways could represent potential chemoprevention agents. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr S5-6.

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