DISACCHARIDASE LEVELS IN IRON DEFICIENT RATS AT BIRTH AND DURING THE NURSING AND POST-WEANING PERIODS - RESPONSE TO IRON TREATMENT

DISACCHARIDASE LEVELS IN IRON DEFICIENT RATS AT BIRTH AND DURING THE NURSING AND POST-WEANING PERIODS - RESPONSE TO IRON TREATMENT
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DOI:
10.1203/00006450-198204000-00016
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发表时间:
1982-01-01
期刊:
影响因子:
3.6
通讯作者:
MILLER, F
MILLER, F
中科院分区:
医学3区
文献类型:
--
作者:
LANZKOWSKY, P;KARAYALCIN, G;MILLER, F

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缺铁母亲(IDM)生下的新生大鼠的汞、蔗糖酶、乳糖酶和麦芽糖酶水平显著低于对照新生大鼠。出生于IDM并由IDM喂养的大鼠21日龄处死时,Hb、血清Fe、蔗糖酶、乳糖酶和麦芽糖酶水平显著低于对照组。出生于IDM但由铁充足的母亲(ISM)喂养并于21日龄处死的大鼠的Hb、血清Fe和蔗糖酶水平与对照组相当,而乳糖酶和麦芽糖酶在ISM喂养21d后仍未纠正。出生于IDM的大鼠接受IDM或ISM喂养21d。右旋糖酐铁,饲喂铁充足饮食(ISD)7天。与对照组大鼠相比,这些动物的汞、血清铁、蔗糖酶和麦芽糖酶水平得到纠正,而肠道乳糖酶在ISD和IM后7天仍未纠正。菲尔。出生于ISM的大鼠、IDM喂养的大鼠和第21天处死的大鼠的Hb、血清Fe和肠道乳糖酶水平显著低于对照组。给ISM出生的大鼠和IDM喂养的大鼠肌肉注射。右旋糖酐铁在第21天,并在第21-28天放置在ISD上。这些动物的Hb、血清铁、蔗糖酶和麦芽糖酶水平与对照组相当。从第21天到84天,由ISM出生和喂养并维持低铁饮食的大鼠的Hb、血清Fe、蔗糖酶、乳糖酶和麦芽糖酶水平显著低于对照组大鼠。从第21天到84天,由ISM出生和喂养的大鼠维持低铁饮食,然后肌肉注射。右旋糖苷铁在第84天持续到第92天,与对照组相比,糖化血红蛋白、血清铁和乳糖酶水平得到纠正。I.M.铁和7天的ISD不能纠正这些大鼠的蔗糖酶和麦芽糖酶水平。与对照组相比,缺铁大鼠的乳糖耐量试验显示出平坦的曲线。铁处理后,乳糖耐量曲线恢复到对照水平。子宫内、哺乳期间和断奶后的大鼠缺铁除了引起贫血外,还会引起空肠二糖酶活性降低,因为刷状缘膜的酶发生了变化。某些双糖对铁处理的不同程度的减少和反应取决于缺铁的时间,这与子宫内和出生后小肠消化和吸收功能的发展有关。二糖水平的变化代表了缺铁所产生的生化效应的另一个方面。铁缺乏对蛋白质合成有深远的影响。双糖水平的变化只代表了这种影响的一小部分。缺铁婴儿乳糖酶和其他二糖酶的暂时性降低可能导致吸收不良和腹泻,这是缺铁婴儿血清蛋白降低和低体重百分位数发生率增加的原因之一。
Newborn rats born to Fe-deficient mothers (IDM) had significantly lower Hg, sucrase, lactase and maltase levels compared to control newborn rats. Rats born to IDM and nursed by IDM, when sacrificed at 21 days of age, had statistically significantly lower Hb, serum Fe, sucrase, lactase and maltase levels compared to control rats. Rats born to IDM but nursed by Fe-sufficient mothers (ISM) and sacrificed at 21 days of age had Hb, serum Fe and sucrase levels comparable to control rats, whereas lactase and maltase were not corrected by 21 days of nursing by ISM. Rats born to IDM and nursed by either IDM or ISM for 21 days were given i.m. iron dextran and placed on Fe-sufficient diet (ISD) for 7 days. These animals experienced correction of the Hg, serum Fe, sucrase and maltase levels compared to control rats, whereas intestinal lactase was not corrected by 7 days of ISD and i.m. Fe. Rats born to ISM, nursed by IDM and sacrificed on day 21 had significantly lower Hb, serum Fe and intestinal lactase levels compared to control rats. Rats born to ISM and nursed by IDM were given i.m. iron dextran on day 21 and placed on an ISD from day 21-28. These animals had a return in Hb, serum Fe, sucrase and maltase levels comparable to control rats. Rats born to and nursed by ISM and maintained on an Fe-deficient diet from day 21-84 had significantly lower Hb, serum Fe, sucrase, lactase and maltase levels compared to control rats. Rats born to and nursed by ISM maintained on Fe-deficient diet from day 21-84 and then given i.m. iron dextran on day 84 and maintained on an ISD until day 92 experienced correction of the Hb, serum Fe and lactase levels compared to control rats. I.m. Fe and 7 days of ISD did not correct the sucrase and maltase levels in these rats. Lactose tolerance tests in Fe-deficient rats showed flat curves compared to controls. After Fe treatment, lactose tolerance curves returned to control values. Fe deficiency in rats in utero, during the nursing and post weaning period causes, in addition to anemia, a reduction in jejunal disaccharidase activity because of an alteration in the enzymes of the brush border membrane. Varying degrees of reduction and response of certain disaccharides to Fe treatment are dependent on the time of Fe deprivation in relationship to the intrauterine and postnatal development of the digestive and absorptive functions in the small intestine. Alterations in the levels of disaccharides represent another aspect of the spectrum of biochemical effects of Fe deficiency. Fe deficiency has a profound effect on protein synthesis. Alterations in the levels of disaccharides represent only a fraction of this effect. The temporary reduction in lactase and other disaccharidases in Fe-deficient infants might predispose them to malabsorption and diarrhea, which contribute to the lowered serum protein and increased incidence of low weight percentiles observed in Fe-deficient infants.