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Swine Nutrition and Feed Technology
Asian-Australasian Journal of Animal Sciences 2006;19(4): 554-562.
https://doi.org/10.5713/ajas.2006.554    Published online February 1, 2006.
Effect of Genotype on Whole-body and Intestinal Metabolic Response to Monensin in Mice
Y.K. Fan*, W.J. Croom, Jr., Linda Daniel, B.W. McBride, M. Koci, G.B. Havenstein, E.J. Eisen
Correspondence:  Y.K. Fan,
Two lines of mice, M16 selected for rapid growth and a randomly selected control ICR as well as their reciprocal crosses were used to study 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 mmol/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 O2 consumption was measured. At the end of two weeks, jejunal O2 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 m, p<0.05), and less jejunal tissue O2 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 O2 consumption per gram of body weight (1.68 vs. 2.11-2.34 mol/min쨌g 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 cm/g FBW, p<0.05), wider villi (109 vs. 87-93 m, p<0.05), more mature height of enterocytes (28.8 vs. 24.4-25.1 m, p<0.05) and a lower rate (91 vs. 133-145 管mol glucose/min??g jejunum, p<0.05) and less energetic efficiency (95 vs. 59-72 管mol ATP expended/管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 O2 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.
Keywords: Intestine; Metabolism; Monensin; Genotype; Growth; Mouse

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