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dc.contributor.authorFan, Y.K.en_US
dc.contributor.authorCroom, W.J.en_US
dc.contributor.authorDaniel, L.en_US
dc.contributor.authorMcBride, B.W.en_US
dc.contributor.authorKoci, M.en_US
dc.contributor.authorHavenstein, G.B.en_US
dc.contributor.authorEisen, E.J.en_US
dc.description.abstractTwo lines of mice, M16 selected for rapid growth and a randomly,elected control ICR as well as their reciprocal crosses were used to stud), the effects of genotype on whole-body energetics and intestinal responses to monensin. Six mice, eight weeks of age, from each line or reciprocal cross were assigned to one of two treatments, 1) drinking water containing 20 mol/l. monensin dissolved in 0.5% V/V ethanol, and 2) drinking water containing 0.5% V/V ethanol (control) for two weeks, After 11 days (age of 9 weeks and 4 days), whole-body O-2 consumption was measured. At the end of two weeks. jejunal O-2 consumption. intestinal tissue composition and histomorphometrics as well as the rate and efficiency of glucose absorption were estimated. In comparison with the control, monensin administration in drinking water resulted in less daily water intake (13.4 vs. 15.5 ml/mouse, p < 0.01), less protein to DNA ratio of jejunal mucosa (5.41 vs. 6.01 mg/mg, p < 0.05), lower villus width (88 vs. 100 mu m. p < 0.05), and less jejunal tissue 0, consumption enhancement by alcohol (7.2 vs. 10.5%, p < 0.01) in mice, Other than those changes, monensin had little (p < 0.05) effect on variables measured in either line of mice or their reciprocal cross, In contrast, the M16 line, selected for rapid growth, as compared to the ICR controls or the reciprocal crosses, had less initial (pre-monensin treatment) whole-body O-2 consumption per grain of body weight (1.68 vs. 2.11-2.34 mu mol/min(.)g BW p < 0.01) as compared to the ICR and reciprocal crosses, In addition, the M16 mice exhibited greater growth (412 vs. 137-210 mg/d, p < 0.05), better feed efficiency (41.7 vs. 19.9-29.3 mg gain/g feed. p, 0,05). shorter small intestines adjusted for fasted body weight (1.00 vs. 1.22-1.44 crn/g FBw, p < 0.05), wider villi (109 vs. 87-93 mu M, p < 0.05), more mature height of enterocytes (28.8 vs. 24.4-25.1 mu m, p < 0.05) and a lower rate (91 vs, 133-145 eta mol glucose/min(.)g jejunum, p < 0.05) and loss energetic efficiency (95 vs. 59-72 eta mol ATP expended/eta mol glucose uptake, p < 0.05) of glucose absorption compared to the ICR line and the reciprocal cross. Monensin had little (p > 0.05) effect on whole-body O-2 consumption and jejunal function, whilst selection for rapid growth resulted in an apparent down-regulation of intestinal function. These data suggest that genetic selection for increased growth does not result in concomitant changes in intestinal function. This asynchrony in the selection for production traits and intestinal function may hinder full phenotypic expression of genotypic growth potential.en_US
dc.relationAsian-Australasian Journal of Animal Sciencesen_US
dc.relation.ispartofseriesAsian-Australasian Journal of Animal Sciences, Volume 19, Issue 4, Page(s) 554-562.en_US
dc.subjectjejunal glucose-absorptionen_US
dc.subjectpolygenic obese miceen_US
dc.subjectadipose cellularityen_US
dc.titleEffect of genotype on whole-body and intestinal metabolic response to monensin in miceen_US
dc.typeJournal Articlezh_TW
item.openairetypeJournal Article-
item.fulltextno fulltext-
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