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      Intestinal Absorption and Biliary Secretion of Zinc in Rats with Chronic Renal Failure

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          Background/Aims: In chronic renal failure (CRF), zinc deficiency is partially attributed to decreased intestinal zinc absorption, but the mechanism of this decrease in intestinal zinc absorption is obscure. Therefore, the objective of this study was to investigate the cause of decreased intestinal zinc absorption in a uremic rat model using an in vivo perfusion technique as well as to evaluate the effect of intestinal zinc perfusion on the secretion of biliary zinc in normal and CRF rats. Methods: CRF was induced by five-sixths nephrectomy (Nx). During zinc sulfate perfusion, absorption of zinc in the small intestine and the response of plasma zinc level were measured. After intestinal zinc perfusion for 80 min, the concentrations of zinc and metallothionein (MT) in the intestinal mucosal and liver tissue were assayed. The secretion of biliary zinc and the excretion of urinary zinc were also determined before and after zinc sulfate perfusion. The results were compared with those obtained from 10 sham-operated normal rats. Results: The CRF rats showed a significant decrease in the rate of intestinal zinc absorption and in the response of plasma zinc levels during intestinal zinc perfusion. They also had significantly higher levels of mucosal zinc and MT than sham-operated normal rats, but their contents of liver zinc were significantly lower than those of sham-operated normal rats after zinc sulfate perfusion. CRF rats showed a low plasma zinc level and a high urinary zinc excretion in baseline levels, but had similar output of basal biliary zinc as compared with sham-operated normal rats. Zinc sulfate perfusion in the small intestinal was not found to increase the secretion of biliary zinc and the excretion of urinary zinc, either in normal or CRF rats. Conclusion: In the CRF rat, the reduction of intestinal zinc absorption may result from reduced mucosal zinc efflux from the basolateral membrane into plasma. These data also suggest that the absorbed zinc from the gastrointestinal tract is mostly taken up by the liver or other tissues, and is less excreted in bile juice and urine.

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          Zinc deficiency in Crohn's disease.

           Joy T. Matsui (1998)
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            A comparison of the short-term kinetics of zinc metabolism in women during fasting and following a breakfast meal.

            The physiological importance and mechanism of the postprandial fall in plasma Zn concentration is not well understood. In order to gain further information on this apparent redistribution of plasma Zn, a stable isotope, 70Zn, was used to study the effect of a breakfast meal on plasma Zn kinetics. Nine women participated in two trials, a fasting trial and a breakfast-meal trial; five of the women participated in a third trial in which the energy content of the breakfast meal was doubled. At each trial, 0.1 mg of 70Zn was infused intravenously, and the plasma disappearance of the isotope was analysed using a two-compartment model of Zn kinetics. Plasma Zn concentration fell significantly following the two trials in which the subjects were given meals, reaching low points that were 13 and 19%, respectively, below concentrations at comparable times during the fasting trial. Kinetic analysis revealed that after the doubled breakfast meal there was a significant fall (P < 0.007) in the size of the most rapidly turning over Zn pool (pool (a)) from 2.90 (SE 0.13) mg in the fasting state to 2.47 (SE 0.14) mg postprandially. The fractional turnover rate of pool (a) to other extravascular Zn pools, i.e. outside the two-compartment system, was also significantly elevated after the doubled breakfast meal (P < 0.05). These results suggest that the decline in plasma Zn concentration following a meal is due to a redistribution of Zn from the plasma to other more slowly turning over extravascular pools that may be involved in the assimilation and metabolism of fuels following food intake.
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              Possible Site of Decreased Intestinal Zinc Absorption in Chronic Uremic Rats

              Background/Aims: Previous zinc tolerance tests in uremic patients indicated decreased intestinal zinc absorption. In the present study, a zinc tolerance test was initially applied to a uremic rat model and subsequently the possible site of malabsorption investigated. Methods: Chronic uremia was induced by five-sixths nephrectomy. Both control and nephrectomized rats were divided into three groups including animals with intact intestine, removal of the jejunum, and removal of the ileum. Each rat was orally loaded with zinc sulfate (80 mg/kg) in conscious state. Blood samples were drawn before and after zinc load at different intervals during 6 h for zinc analysis. The area under the plasma zinc curve (AUC) and the maximal increase of plasma zinc level (C max ) were calculated. Results: Jejunectomy decreased both AUC and C max in control and nephrectomized rats, whereas ileectomized animals remained, interestingly, unchanged with regard to these two parameters. Significant decreases in both AUC and C max were observed in nephrectomized rats as compared with the control rats. Conclusions: The jejunum is the main site of zinc absorption in response to a large oral load of zinc sulfate in both normal and uremic rats. The data further suggest that five-sixths nephrectomy reduces gastrointestinal zinc absorption in rats predominantly by the ileum.

                Author and article information

                Nephron Physiol
                Nephron Physiology
                S. Karger AG
                April 2004
                30 April 2004
                : 96
                : 4
                : p113-p120
                aDepartment of Medical Research and Education, Nephrology Laboratory, Taipei Veterans General Hospital, bDepartment of Pharmacology, National Yang-Ming University, and cDepartment of Medical Research and Education, Metabolism Laboratory, Taipei Veterans General Hospital, Taipei, Taiwan/ROC
                77382 Nephron Physiol 2004;96:p113–p120
                © 2004 S. Karger AG, Basel

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                Page count
                Figures: 5, Tables: 1, References: 53, Pages: 1
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/77382
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