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Feeding Mice (feeding + mouse)
Selected AbstractsAnti-Inflammatory and Anti-Apoptotic Roles of Endothelial Cell STAT3 in Alcoholic Liver InjuryALCOHOLISM, Issue 4 2010Andrew M. Miller Background:, It is generally believed that the hepatoprotective effect of interleukin-6 (IL-6) is mediated via activation of signal transducer and activator of transcription 3 (STAT3) in hepatocytes. IL-6-deficient mice are more susceptible to alcohol-induced hepatocyte apoptosis and steatosis and elevation of serum alanine transaminase (ALT); however, whereas hepatocyte-specific STAT3 knockout mice are more susceptible to alcohol-induced hepatic steatosis, they have similar hepatocyte apoptosis and serum ALT after alcohol feeding compared with wild-type mice. This suggests that the hepatoprotective effect of IL-6 in alcoholic liver injury may be mediated via activation of STAT3-independent signals in hepatocytes, activation of STAT3 in nonparenchymal cells, or both. We have previously shown that IL-6 also activates STAT3 in sinusoidal endothelial cells (SECs). Thus, the purpose of this study was to investigate whether STAT3 in endothelial cells also plays a protective role in alcoholic liver injury. Methods:, Wild-type and endothelial cell-specific STAT3 knockout (STAT3E,/,) mice were pair-fed and fed ethanol containing diet for 4 weeks. Liver injury and inflammation were determined. Results:, Feeding mice with ethanol-containing diet for 4 weeks induced greater hepatic injury (elevation of serum ALT) and liver weight in STAT3E,/, mice than wild-type control groups. In addition, ethanol-fed STAT3E,/, mice displayed greater hepatic inflammation and substantially elevated serum and hepatic levels of IL-6 and TNF-, compared with wild-type mice. Furthermore, ethanol-fed STAT3E,/, mice displayed a greater abundance of apoptotic SECs and higher levels of serum hyaluronic acid than wild-type controls. Conclusions:, These data suggest that endothelial cell STAT3 plays important dual functions of attenuating hepatic inflammation and SEC death during alcoholic liver injury. [source] The influence of dietary linoleic and , -linolenic acid on body composition and the activities of key enzymes of hepatic lipogenesis and fatty acid oxidation in mice,JOURNAL OF ANIMAL PHYSIOLOGY AND NUTRITION, Issue 1-2 2007M. Javadi Summary We have recently suggested that feeding the C18 polyunsaturated fatty acid, , -linolenic acid (ALA), instead of linoleic acid (LA) reduced body fat in mice. However, the difference in body fat did not reach statistical significance, which prompted us to carry out this study using more animals and diets with higher contents of ALA and LA so that the contrast would be greater. The diets contained either 12% (w/w) LA and 3% ALA or 12% ALA and 4% LA. A low-fat diet was used as control. The diets were fed for 35 days. The proportion of body fat was not influenced by the type of dietary fatty acid. Plasma total cholesterol and phospholipids were significantly lower in ALA-fed mice than in mice fed LA. Activities of enzymes in the fatty acid oxidation pathway were significantly raised by these two diets when compared with the control diet. , -Linolenic acid vs. LA did not affect fatty acid oxidation enzymes. In mice fed the diet with LA activities of enzymes of de novo fatty acid synthesis were significantly decreased when compared with mice fed the control diet. , -Linolenic acid vs. LA feeding did not influence lipogenic enzymes. It is concluded that feeding mice for 35 days with diets either rich in LA or ALA did not significantly influence body composition. [source] Expression of aquaporins in the efferent ductules, sperm counts, and sperm motility in estrogen receptor-, deficient mice fed lab chow versus caseinMOLECULAR REPRODUCTION & DEVELOPMENT, Issue 2 2006Ricardo Ruz Abstract Estrogens play an important role in the male reproductive tract, and this is especially so for the efferent ductules, where ,-estrogen receptors (ER,) have been localized. Mice deficient in ER, (,ERKO mice) are infertile, and the effect appears to be due in part to retention of water at the level of the efferent ductules. In the present study, we examined the consequences of ER, deletion on the distribution of certain aquaporins (AQPs), water protein channels, in the efferent ductules and on sperm numbers and motility. In addition, the effects of feeding mice a regular lab chow diet, which contains phytoestrogens, known to affect male reproductive tract functions, and a casein diet, which lacks phytoestrogens, were also assessed. Light microscope immunolocalizations of AQP-1 and AQP-9 revealed dramatic reduction and patchier staining in ,ERKO mice with distal areas of the efferent ductules being more affected than proximal areas. No other changes in immunolocalizations were noted as a consequence of diet. Computer-assisted sperm analyses demonstrated a 62% reduction in cauda epididymal sperm/ml in ,ERKO mice fed lab chow, whereas 87% fewer sperm/ml were observed in ,ERKO mice fed casein, suggesting an enhanced role for sperm production and concentration in a diet containing phytoestrogens. All sperm motility parameters were altered to some degree in ,ERKO mice fed lab chow. Alterations in sperm motility parameters were also detected, but were less dramatic in ,ERKO mice fed casein. These data suggest that the decrease in AQP expression in the efferent ductules of ,ERKO mice contributes in part to water retention in this tissue, eventually leading to backflow of water into the testis, with subsequent decreases in sperm concentration and motility. The data also suggest that phytoestrogens, which are present in regular lab chow, can influence the male reproductive tract with and without the presence of ER,, promoting efferent ductule and epididymal functions when ER, is expressed, but inhibiting these same functions when ER, is missing. Taken together the data underscore the importance of estrogens and ER, in maintaining sperm maturation and preventing male infertility. Mol. Reprod. Dev. © 2005 Wiley-Liss, Inc. [source] Experimental pancreatitis disturbs gastrointestinal and colonic motility in mice: effect of the prokinetic agent tegaserodNEUROGASTROENTEROLOGY & MOTILITY, Issue 10 2007T. C. Seerden Abstract, Acute pancreatitis remains a potentially life-threatening disease associated with gastrointestinal motility disturbances. Prokinetic agents may be useful to overcome these motility disturbances. In this study, we investigated the effect of acute necrotizing pancreatitis (ANP) on gastrointestinal motility in female mice and evaluated the effect of tegaserod, a prokinetic 5-hydroxytryptamine-4 (5HT4) receptor agonist. ANP was induced by feeding mice a choline-deficient ethionine-supplemented diet during 72 h. In vivo intestinal motility was measured as the geometric centre (GC) of 25 glass beads 30-120-360 min after gavage. Colonic peristaltic activity was studied using a modified Trendelenburg set-up. ANP significantly decreased GC 30-120-360 min after bead gavage, associated with a significant increase of myeloperoxidase in the proximal small intestine and colon, but not in the stomach or distal small intestine. Tegaserod significantly ameliorated GC 360 min after bead gavage in control and pancreatitis mice. In isolated colonic segments, ANP significantly decreased the amplitude of peristaltic waves and increased the interval between peristaltic contractions. Tegaserod normalized the disturbed interval. In conclusion, ANP impairs gastric, small intestinal and colonic motility in mice. Tegaserod improves ANP-induced motility disturbances in vivo and in vitro, suggesting a therapeutic benefit of prokinetic 5HT4 receptor agonists in the treatment of pancreatitis-induced ileus. [source] The Effects of Inhibition of Haem Biosynthesis by Griseofulvin on Intestinal Iron AbsorptionBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 4 2004Abas H. Laftah Urinary 5-aminolaevulinic acid levels were increased within 24 hr of feeding mice with griseofulvin diet (2.5% w/w), with more marked increases seen after 3,7 days. Urinary porphobilinogen levels also showed a similar trend. In vivo intestinal iron absorption was significantly reduced (P<0.05) in experimental mice, mainly due to reduction in the transfer of 59Fe from the enterocytes to the portal circulation. In vitro studies using isolated duodenal fragments also exhibited marked decreases in both iron uptake and Fe (III) reduction. Changes in mucosal Divalent Metal Transporter 1 (DMT-1), Dcytb and Ireg1 (iron regulated protein 1) mRNA levels paralleled the changes in iron absorption. The reduction in iron absorption after griseofulvin treatment was normalised when mice were simultaneously injected with haem-arginate. These data support the hypothesis that intermediates in haem biosynthesis, particularly 5-aminolaevulinic acid, regulate intestinal iron absorption. [source] | |||||||||||||