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大鼠小肠肌酸摄取的发育性降低。

Developmental decrease in rat small intestinal creatine uptake.

作者信息

Peral M J, Gálvez M, Soria M L, Ilundáin A A

机构信息

Departamento de Fisiología y Zoología, Facultad de Farmacia, Universidad de Sevilla, C/Garcia Gonzalez no. 2, 41012 Sevilla, Spain.

出版信息

Mech Ageing Dev. 2005 Apr;126(4):523-30. doi: 10.1016/j.mad.2004.11.005. Epub 2004 Dec 22.

Abstract

Phosphocreatine is an energy buffer and transducer in the heart, the brain and the skeletal muscle. Recently, we have demonstrated the presence of the Na+/Cl-/creatine transporter at the apical membrane of the small intestinal epithelium. Herein the ontogeny and segmental distribution of rat intestinal creatine transport activity are investigated. [14C]-Creatine uptake was measured in the jejunum and ileum of 16 day gestation foetuses, newborn, suckling, weaning, 1-, 2-, 7- and 12-month-old (adult) rats. Creatine content in amniotic fluid, in rat and commercial milk and in rat chow, was measured by HPLC. NaCl-dependent creatine uptake was maximal in newborn rats and, in all the ages tested, higher in the ileum than in the jejunum. In the latter, NaCl-dependent creatine uptake was undetectable after weaning. Kinetic studies revealed that the jejunum and ileum have the same creatine uptake system, and that maturation decreases its Vmax but not the apparent Km. Maintenance of the pups on a commercial milk diet supplemented with creatine prevented the ileal periweaning decline in creatine uptake activity, but not that in the jejunum. In 1-month-old rats, supplementation with creatine increased ileal, but not jejunal, creatine uptake. The results demonstrate for the first time that: (i) creatine uptake along the length of the small intestine is mediated by the same transport system, (ii) the activity of this transport system changes in a specific manner with maturation and (iii) these changes appear to be genetically programmed and controlled by the intestinal creatine content.

摘要

磷酸肌酸是心脏、大脑和骨骼肌中的一种能量缓冲剂和转换器。最近,我们已经证明在小肠上皮细胞的顶端膜存在钠/氯/肌酸转运体。在此研究了大鼠肠道肌酸转运活性的个体发生和节段分布。测量了妊娠16天胎儿、新生、哺乳、断奶、1个月、2个月、7个月和12个月大(成年)大鼠空肠和回肠中[14C] - 肌酸的摄取量。通过高效液相色谱法测量羊水、大鼠和市售牛奶以及大鼠饲料中的肌酸含量。依赖氯化钠的肌酸摄取在新生大鼠中最大,并且在所有测试年龄中,回肠中的摄取量高于空肠。在空肠中,断奶后依赖氯化钠的肌酸摄取无法检测到。动力学研究表明,空肠和回肠具有相同的肌酸摄取系统,并且成熟会降低其Vmax但不会降低表观Km。用补充了肌酸的市售牛奶喂养幼崽可防止回肠断奶前后肌酸摄取活性的下降,但不能防止空肠中的下降。在1个月大的大鼠中,补充肌酸可增加回肠而非空肠的肌酸摄取。结果首次证明:(i)沿小肠长度的肌酸摄取由相同的转运系统介导,(ii)该转运系统的活性随成熟以特定方式变化,以及(iii)这些变化似乎是由基因编程并受肠道肌酸含量控制的。

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