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        Development of a Dynamic System Simulating Pig Gastric Digestion

        Chiang, C.-C.,Croom, J.,Chuang, S.-T.,Chiou, P.W.S.,Yu, B. Asian Australasian Association of Animal Productio 2008 Animal Bioscience Vol.21 No.10

        The objective of this study was to develop a model for simulating gastric digestion in the pig. The model was constructed to include the chemical and physical changes associated with gastric digestion such as enzyme release, digestion product removal and gastric emptying. Digesta was collected from the stomach cannula of pigs to establish system parameters and to document the ability of the model to simulate gastric digestion. The results showed that the average pH of gastric digesta increased significantly from 2.47 to 4.97 after feed consumption and then decreased 140 min postprandial. The model described the decrease in pH within the pigs' stomach as $pH_t=5.182e^{-0.0014t}$, where t represents the postprandial time in minutes. The cumulative distribution function of liquid digesta was $V_t=64.509e^{0.0109t}$. The average pepsin activity in the liquid digesta was 317Anson units/mL. There was significant gastric emptying 220 min after feed consumption. The cybernetic dynamic system of gastric digestion was set according to the above data in order to compare with in vivo changes. The time course of crude protein digestion predicted by the model was highly correlated with observed in vivo digestion (r = 0.97; p = 0.0001), Model prediction for protein digestion was higher than that observed for a traditional static in vitro method (r = 0.89; p = 0.0001).

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        Effect of Genotype on Whole-body and Intestinal Metabolic Response to Monensin in Mice

        Fan, Y.K.,Croom, W.J.,Daniel, Linda,McBride, B.W.,Koci, M.,Havenstein, G.B.,Eisen, E.J. Asian Australasian Association of Animal Productio 2006 Animal Bioscience Vol.19 No.4

        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 $O_2$ 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 $O_2$ 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 gram of body weight (1.68 vs. $2.11-2.34{\mu}mol/min{\cdot}g$ 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 cm/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. $133-145{\eta}mol\;glucose/min{\cdot}g$ jejunum, p<0.05) and less 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.

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