Monensin and<sup>14</sup>C oleic acid absorption in the rat

Hussenet, M. P.; Pavero, Catherine; Bernard, Alain; Carlier, H.

doi:10.1080/02652039009373874

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“…In contrast, Raja et al (1989) reported that the ionophore, valinomycin, increased glucose uptake in the mouse duodenum. There have been reports that monensin decreased oleic acid absorption in rat enterocytes (Husenet et al, 1990) and intestinal cholesterol uptake from cultured human intestine (Sviridov et al, 1993). Our laboratory failed to find any effects of the ionophore antibiotics, laidlomycin, laidlomycin propionate or monensin on wholebody energy metabolism or jejunal function of Swiss Webster mice (Fan et al, 2003).…”

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confidence: 62%

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

Fan¹,

Croom²,

Daniel³

et al. 2006

Asian Australas. J. Anim. Sci

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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 µm, 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 µmol/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 cm/g FBW, p<0.05), wider villi (109 vs. 87-93 µm, p<0.05), more mature height of enterocytes (28.8 vs. 24.4-25.1 µm, p<0.05) and a lower rate (91 vs. 133-145 ηmol glucose/min⋅g jejunum, p<0.05) and less energetic efficiency (95 vs. 59-72 ηmol ATP expended/ηmol 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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