Fructose-1,6-bisphosphate as a metabolic substrate in hog ileum smooth muscle during hypoxia.
Fructose-1,6-bisphosphate as a metabolic substrate in hog ileum smooth muscle during hypoxia.
复制标题
1,6-二磷酸果糖作为缺氧期间猪回肠平滑肌的代谢底物。
DOI：
10.1007/bf00248465
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发表时间：
1996
影响因子：
4.3
通讯作者：
Hardin,CD
中科院分区：
文献类型：
--
作者：
Juergens,TM;Hardin,CD
外源性应用果糖-1,6-二磷酸已报道有效防止小肠缺血时的一些损伤。为了确定外源性果糖-1,6-二磷酸是否能保护回肠平滑肌免受缺氧和再氧化的损伤，我们研究了果糖-1,6-二磷酸对猪回肠平滑肌在缺氧时维持等距力和在5毫米葡萄糖存在下再氧化后产生等距力的能力的影响。缺氧180分钟后，用20 mM果糖-1,6-二磷酸盐孵育的组织比没有外源性底物孵育的组织维持的等长力水平明显更高（缺氧前力的23%与16%相比）。在再氧化后的第一次收缩期间，与缺氧期间不含外源性底物的组织相比，在缺氧期间用20 mM果糖-1,6-二磷酸孵育的组织产生的力明显更大（缺氧前力的29%与19%相比）。然而，在所有实验条件下，葡萄糖总是比果糖-1,6-二磷酸更好的代谢底物。在缺氧期间，果糖-1,6-二磷酸的存在可能通过果糖-1,6-二磷酸进入细胞并作为糖酵解的中间体来改善组织功能，因为在120分钟的缺氧期间，未安装的回肠平滑肌将1,6- 13c -果糖-1,6-二磷酸代谢为3- 13c -乳酸。1,6- 13c -果糖-1,6-二磷酸转化为3- 13c -乳酸的过程被加入1mm的碘乙酸（糖酵解抑制剂）所抑制。我们得出结论，外源性提供的果糖-1,6-二磷酸确实通过作为糖酵解中间体和改善细胞能量状态，对回肠平滑肌缺氧损伤提供适度的保护。
Exogenously applied fructose-1,6-bisphosphate has been reported to be effective in preventing some damage to the small intestine during ischemia. To determine whether exogenously applied fructose-1,6-bisphosphate protects ileum smooth muscle from damage from hypoxia and from reoxygenation, we examined the effect of fructose-1,6-bisphosphate on the ability of hog ileum smooth muscle to maintain isometric force during hypoxia and to generate isometric force after reoxygenation in the presence of 5 mM glucose. After 180 min of hypoxia, tissues incubated with 20 mM fructose-1,6-bisphosphate maintained significantly greater levels of isometric force than tissues incubated in the absence of exogenous substrate (23% of pre-hypoxia force compared to 16%). During the first contraction following reoxygenation there was a significantly greater force generation in tissues incubated with 20 mM fructose-1,6-bisphosphate during the hypoxia period compared to tissues with no exogenous substrate included during the hypoxia period (29% of pre-hypoxia force compared to 19%). However, glucose always was a better metabolic substrate compared to fructose-1,6-bisphosphate under all experimental conditions. The presence of fructose-1,6-bisphosphate during hypoxia likely improved tissue function by fructose-1,6-bisphosphate entering the cells and acting as a glycolytic intermediate, since during a 120 min period of hypoxia, unmounted ileum smooth muscle metabolized 1,6-13C-fructose-1,6-bisphosphate to 3-13C-lactate. This conversion of 1,6-13C-fructose-1,6-bisphosphate to 3-13C-lactate was inhibited by the addition of 1 mM iodoacetic acid, a glycolytic inhibitor. We conclude that exogenously provided fructose-1,6-bisphosphate does provide modest protection of ileum smooth muscle from hypoxic damage by functioning as a glycolytic intermediate and improving the cellular energy state.