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<title>Faculty Research Publications (Animal Science)</title>
<link>http://hdl.handle.net/1957/30112</link>
<description/>
<pubDate>Wed, 19 Jun 2013 11:59:38 GMT</pubDate>
<dc:date>2013-06-19T11:59:38Z</dc:date>
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<title>Fructokinase, Fructans, Intestinal Permeability, and Metabolic Syndrome: An Equine Connection?</title>
<link>http://hdl.handle.net/1957/38037</link>
<description>Fructokinase, Fructans, Intestinal Permeability, and Metabolic Syndrome: An Equine Connection?
Johnson, Richard J.; Rivard, Chris; Lanaspa, Miguel A.; Otabachian-Smith, Silvia; Ishimoto, Takuji; Cicerchi, Christina; Cheeke, Peter R.; McIntosh, Bridgett; Hess, Tanja
Fructose is a simple sugar present in honey and fruit, but can also exist as a polymer (fructans) in pasture grasses. Mammals are unable to metabolize fructans, but certain gram positive bacteria contain fructanases and can convert fructans to fructose in the gut. Recent studies suggest that fructose generated from bacteria, or directly obtained from the diet, can induce both increased intestinal permeability and features of metabolic syndrome, especially the development of insulin resistance. The development of insulin resistance is driven in part by the metabolism of fructose by fructokinase C in the liver, which results in oxidative stress in the hepatocyte. Similarly, the metabolism of fructose in the small bowel by intestinal fructokinase may lead to increased intestinal permeability and endotoxemia. While speculative, these observations raise the possibility that the mechanism by which fructans induce laminitis could involve intestinal and hepatic fructokinase. Further studies are indicated to determine the role of fructanases, fructose and fructokinase in equine metabolic syndrome and laminitis.
This is the author's peer-reviewed final manuscript, as accepted by the publisher. The published article is copyrighted by Elsevier and can be found at: http://www.journals.elsevier.com/journal-of-equine-veterinary-science/.
</description>
<pubDate>Fri, 01 Feb 2013 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/1957/38037</guid>
<dc:date>2013-02-01T00:00:00Z</dc:date>
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<title>Selenium and Selenoprotein Deficiencies Induce Widespread Pyogranuloma Formation in Mice, while High Levels of Dietary Selenium Decrease Liver Tumor Size Driven by TGFa</title>
<link>http://hdl.handle.net/1957/38031</link>
<description>Selenium and Selenoprotein Deficiencies Induce Widespread Pyogranuloma Formation in Mice, while High Levels of Dietary Selenium Decrease Liver Tumor Size Driven by TGFa
Moustafa, Mohamed E.; Carlson, Bradley A.; Anver, Miriam R.; Bobe, Gerd; Zhong, Nianxin; Ward, Jerrold M.; Perella, Christine M.; Hoffmann, Victoria J.; Rogers, Keith; Combs, Gerald F. Jr.; Schweizer, Ulrich; Merlino, Glenn; Gladyshev, Vadim N.; Hatfield, Dolph L.
Changes in dietary selenium and selenoprotein status may influence both anti- and pro-cancer pathways, making the outcome of interventions different from one study to another. To characterize such outcomes in a defined setting, we undertook a controlled hepatocarcinogenesis study involving varying levels of dietary selenium and altered selenoprotein status using mice carrying a mutant (A37G) selenocysteine tRNA transgene (Trsp[superscript tG37]) and/or a cancer driver TGFα transgene. The use of Trsp[superscript tG37] altered selenoprotein expression in a selenoprotein and tissue specific manner and, at sufficient dietary selenium levels, separate the effect of diet and selenoprotein status. Mice were maintained on diets deficient in selenium (0.02 ppm selenium) or supplemented with 0.1, 0.4 or 2.25 ppm selenium or 30 ppm triphenylselenonium chloride (TPSC), a non-metabolized selenium compound. Trsp[superscript tG37] transgenic and TGFα/Trsp[superscript tG37] bi-transgenic mice subjected to selenium-deficient or TPSC diets developed a neurological phenotype associated with early morbidity and mortality prior to hepatocarcinoma development. Pathology analyses revealed widespread disseminated pyogranulomatous inflammation. Pyogranulomas occurred in liver, lungs, heart, spleen, small and large intestine, and mesenteric lymph nodes in these transgenic and bi-transgenic mice. The incidence of liver tumors was significantly increased in mice carrying the TGFα transgene, while dietary selenium and selenoprotein status did not affect tumor number and multiplicity. However, adenoma and carcinoma size and area were smaller in TGF alpha transgenic mice that were fed 0.4 and 2.25 versus 0.1 ppm of selenium. Thus, selenium and selenoprotein deficiencies led to widespread pyogranuloma formation, while high selenium levels inhibited the size of TGFα-induced liver tumors.
To the best of our knowledge, one or more authors of this paper were federal employees when contributing to this work.&#13;
This is the publisher’s final pdf. The published article is copyrighted by Public Library of Science and can be found at: http://www.plos.org/.
</description>
<pubDate>Wed, 27 Feb 2013 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/1957/38031</guid>
<dc:date>2013-02-27T00:00:00Z</dc:date>
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<title>Comparison of Bite-Count and Rumen Evacuation Techniques to Estimate Cattle Diet Quality</title>
<link>http://hdl.handle.net/1957/37283</link>
<description>Comparison of Bite-Count and Rumen Evacuation Techniques to Estimate Cattle Diet Quality
Damiran, Daalkhaijav; DelCurto, Timothy; Findholt, Scott L.; Johnson, Bruce K.; Vavra, Martin
We conducted a study to compare the bite-count technique (BC) of estimating forage intake and synthesized diet quality to direct estimates of diet quantity and quality with the use of the rumen evacuation technique (RE). We used four rumen-fistulated steers to evaluate both techniques. Four enclosures in a mixed-conifer rangeland were used. Each enclosure contained two 0.25-ha paddocks that were either nonstocked or stocked by cattle to remove 32 ± 4% of standing crop. We recorded bite-count data during foraging bouts for each steer in each paddock, and then evacuated each rumen following each foraging bout during summer (August). Paddocks stocked prior to each 20-min trial had a reduced (P &lt; 0.05) quantity of forage consumed regardless of technique. BC and RE gave similar (P &gt; 0.10) results on diet quantity and digestibility. However, BC-derived estimates were lower (P &lt; 0.05) for crude protein (CP), acid detergent fiber (ADF), ash, and neutral detergent fiber (NDF). In summary, although BC has the advantage of not requiring rumen-fistulated animals, it did not yield comparable results to RE under range conditions with dense and diverse vegetation. Therefore, investigators should calibrate bite-count technique against fistula technique to solve any accuracy problem in their specific experimental conditions whenever possible.
To the best of our knowledge, one or more authors of this paper were federal employees when contributing to this work.&#13;
This is the publisher’s final pdf. The published article is copyrighted by The Society for Range Management and can be found at: http://www.rangelands.org/.
</description>
<pubDate>Tue, 01 Jan 2013 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/1957/37283</guid>
<dc:date>2013-01-01T00:00:00Z</dc:date>
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<title>Effects of camelina meal supplementation on ruminal forage degradability, performance, and physiological responses of beef cattle</title>
<link>http://hdl.handle.net/1957/35717</link>
<description>Effects of camelina meal supplementation on ruminal forage degradability, performance, and physiological responses of beef cattle
Cappellozza, B. I.; Cooke, R. F.; Bohnert, D. W.; Cherian, G.; Carroll, J. A.
Three experiments compared ruminal, physiological, and performance responses of beef steers consuming hay ad libitum and receiving grain-based supplements without (control) or with (CAM) the inclusion of camelina meal. In Exp. 1, 9 steers fitted with ruminal cannulas received CAM (2.04 kg of DM/d; n = 5) or control (2.20 kg of DM/d; n = 4). Steers receiving CAM had reduced (P = 0.01) total DMI and tended to have reduced (P = 0.10) forage DMI compared with control. No treatment effects were detected (P ≥ 0.35) for ruminal hay degradability parameters. In Exp. 2, 14 steers fed CAM (1.52 kg of DM/d; n = 7) or control (1.65 kg of DM/d; n = 7) were assigned to a corticotropin-releasing hormone (CRH; 0.1 μg/kg of BW) and a thyrotropin-releasing hormone (TRH; 0.33 μg/kg of BW) challenge. Steers fed CAM had greater (P &lt; 0.05) serum concentrations of PUFA compared with control before challenges. Upon CRH infusion, plasma haptoglobin concentrations tended (P = 0.10) to be reduced and ceruloplasmin concentrations increased at a lesser rate in CAM steers compared with control (treatment × time; P &lt; 0.01). Upon TRH infusion, no treatment effects were detected (P ≥ 0.55) for serum thyrotropin-stimulating hormone, triiodothyronine, and thyroxine. In Exp. 3, 60 steers were allocated to 20 pens. Pens were assigned randomly to receive CAM (2.04 kg of DM/steer daily; n = 10) or control (2.20 kg of DM/steer daily; n = 10) during preconditioning (PC; d −28 to 0). On d 0, steers were transported for 24 h. Upon arrival, pens were assigned randomly to receive CAM or control during feedlot receiving (FR; d 1 to 29). During PC, CAM steers had reduced (P &lt; 0.01) forage and total DMI, and tended to have reduced (P = 0.10) ADG compared with control. Plasma linolenic acid concentrations increased during PC for CAM steers, but not for control (treatment × day; P = 0.02). During FR, steers fed CAM during PC had reduced (P &lt; 0.01) forage and total DMI, but tended (P = 0.10) to have greater G:F compared with control. Steers fed CAM during FR had greater (P &lt; 0.05) plasma concentrations of PUFA, and reduced rectal temperature and concentrations of haptoglobin and ceruloplasmin during FR compared with control. In summary, CAM supplementation to steers impaired forage and total DMI, did not alter thyroid gland function, increased circulating concentrations of PUFA, and lessened the acute-phase protein reaction elicited by neuroendocrine stress responses.
This is the publisher’s final pdf. The published article is copyrighted by the American Society of Animal Science and can be found at: http://journalofanimalscience.org/.&#13;
To the best of our knowledge, one or more authors of this paper were federal employees when contributing to this work.
</description>
<pubDate>Thu, 01 Nov 2012 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/1957/35717</guid>
<dc:date>2012-11-01T00:00:00Z</dc:date>
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