Dietary supplementation with hydrolyzed yeast and its effect on the performance, intestinal microbiota, and immune response of weaned piglets.

The objective of this study was to evaluate the effects of autolyzed yeast on performance, cecal microbiota, and leukogram of weaned piglets. A total of 96 piglets of commercial line weaned at 21-day-old were used. The experimental design was a randomized block design with four treatments (diets containing 0.0%, 0.3%, 0.6%, and 0.9% autolyzed yeast), eight replicates, and three animals per pen in order to evaluate daily weight gain, daily feed intake, and feed conversion in periods of 0 to 15, 0 to 26, and 0 to 36 days. Quadratic effects of autolyzed yeast inclusion were observed on the feed conversion from 0 to 15 days, on daily weight gain from 0 to 15 days, 0 to 26 days and, 0 to 36 days, indicating an autolyzed yeast optimal inclusion level between 0.4% and 0.5%. No effect from autolyzed yeast addition was observed on piglet daily feed intake, cecal microbiota, and leukogram; however, i.m. application of E. coli lipopolysaccharide reduced the values of total leukocytes and their fractions (neutrophils, eosinophils, lymphocytes, monocytes, and rods). Therefore, autolyzed yeast when provided at levels between 0.4% and 0.5% improved weaned piglets’ performance.info:eu-repo/semantics/publishedVersio

Estrogen-induced DNA synthesis in vascular endothelial cells is mediated by ROS signaling

<p>Abstract</p> <p>Background</p> <p>Since estrogen is known to increase vascular endothelial cell growth, elevated estrogen exposure from hormone replacement therapy or oral contraceptives has the potential to contribute in the development of abnormal proliferative vascular lesions and subsequent thickening of the vasculature. How estrogen may support or promote vascular lesions is not clear. We have examined in this study whether estrogen exposure to vascular endothelial cells increase the formation of reactive oxygen species (ROS), and estrogen-induced ROS is involved in the growth of endothelial cells.</p> <p>Methods</p> <p>The effect of estrogen on the production of intracellular oxidants and the role of estrogen-induced ROS on cell growth was studied in human umbilical vein endothelial cells. ROS were measured by monitoring the oxidation of 2'7'-dichlorofluorescin by spectrofluorometry. Endothelial cell growth was measured by a colorimetric immunoassay based on BrdU incorporation into DNA.</p> <p>Results</p> <p>Physiological concentrations of estrogen (367 fmol and 3.67 pmol) triggered a rapid 2-fold increase in intracellular oxidants in endothelial cells. E2-induced ROS formation was inhibited to basal levels by cotreatment with the mitochondrial inhibitor rotenone (2 μM) and xanthine oxidase inhibitor allopurinol (50 μM). Inhibitors of NAD(P)H oxidase, apocynin and DPI, did not block E2-induced ROS formation. Furthermore, the NOS inhibitor, L-NAME, did not prevent the increase in E2-induced ROS. These findings indicate both mitochondria and xanthine oxidase are the source of ROS in estrogen treated vascular endothelial cells. E2 treated cells showed a 2-fold induction of BrdU incorporation at 18 h which was not observed in cells exposed to vehicle alone. Cotreatment with ebselen (20 μM) and NAC (1 mM) inhibited E2-induced BrdU incorporation without affecting the basal levels of DNA synthesis. The observed inhibitory effect of NAC and ebselen on E2-induced DNA synthesis was also shown to be dose dependent.</p> <p>Conclusion</p> <p>We have shown that estrogen exposure stimulates the rapid production of intracellular ROS and they are involved in growth signaling of endothelial cells. It appears that the early estrogen signaling does not require estrogen receptor genomic signaling because we can inhibit estrogen-induced DNA synthesis by antioxidants. Findings of this study may further expand research defining the underlying mechanism of how estrogen may promote vascular lesions. It also provides important information for the design of new antioxidant-based drugs or new antioxidant gene therapy to protect the cardiovascular health of individuals sensitive to estrogen.</p

Role of Gα 12-and Gα 13-protein subunit linkage of D \u3csub\u3e3\u3c/sub\u3e dopamine receptors in the natriuretic effect of D \u3csub\u3e3\u3c/sub\u3e dopamine receptor in kidney

The D 3 dopamine receptor is the major D 2-like receptor that regulates sodium transport in the renal proximal tubule (RPT) and helps maintain blood pressure in the normal range. In Wistar-Kyoto (WKY) rats chronically fed high-salt diet, the intrarenal arterial infusion of a D 3 receptor agonist, PD128907, increased absolute and fractional sodium excretion. We have reported that Gα 12 and Gα 13, which participate in the signal transduction of the D 5 receptor, are expressed in RPTs. As the D 3 receptor is also expressed in RPTs, we hypothesized that it may also interact with Gα 12/Gα 13 in RPTs from WKY rats. There were co-localization and co-immunoprecipitation of D 3 receptor and Gα 12/Gα 13 in renal brush border membranes (BBMs) and RPT cells. The intrarenal infusion of PD128907 (1 μg kg -1 min -1) that increased sodium excretion also increased the co-immunoprecipitations of D 3/Gα 12 and D 3/Gα 13 in renal BBMs; their co-immunoprecipitation was confirmed in RPT cells. As Gα 12 and Gα 13 increase sodium pump and transporter activity (for example, Na +-K +-ATPase, NHE3), an increased association of D 3 receptors with Gα 12/Gα 13 receptors after D 3 receptor activation may be a mechanism to prevent Gα 12/Gα 13-mediated stimulation of sodium transport (and thus enhance natriuresis). We conclude that a D 3 receptor interaction with Gα 12/Gα 13 that increases sodium excretion may have a role in the regulation of blood pressure. © 2011 The Japanese Society of Hypertension All rights reserved