Exogenous fructose-1,6-bisphosphate is a metabolizable substrate for the isolated normoxic rat heart
Exogenous fructose-1,6-bisphosphate is a metabolizable substrate for the isolated normoxic rat heart
复制标题
外源性果糖 1,6-二磷酸是离体常氧大鼠心脏的可代谢底物
DOI：
--
复制
发表时间：
1992
影响因子：
9.5
通讯作者：
Bruno Giardina
中科院分区：
文献类型：
--
作者：
B. Tavazzi;Joseph W. Starnes;G. Lazzarino;D. Pierro;E. Nuutinen;Bruno Giardina
在正常条件下，采用Langendorff模式灌注离体大鼠心脏60 min。在克雷布斯-林格缓冲液中加入10mM葡萄糖+ 12iu /l胰岛素和[U-14C]-果糖-1,6-二磷酸（连同5mm冷果糖-1,6-二磷酸）或[U-14C]-果糖（连同5mm冷果糖）。灌注结束时，测定两组心脏的气体14CO2、灌注液中捕获的14CO2、14c -乳酸输出量和组织14c -乳酸。对冷冻夹心的中和过氯酸提取物也进行了高能化合物、糖原、乳酸和丙酮酸的分析。来自放射性标记底物代谢的14c分解代谢物的数据表明，离体的常氧大鼠心脏代谢果糖-1,6-二磷酸（7.07 μmol /min/g d.w.）的量是果糖（0.83 μmol /min/g d.w.）的8.5倍。在果糖-1,6-二磷酸盐灌注的心脏中，组织和灌注液中的CrP、CrP/Cr、糖原和总乳酸水平均显著升高。综上所述，果糖-1,6-二磷酸可以以完整的形式被肌细胞吸收，并连续代谢以支持其能量需求，其对心肌性能和代谢的影响应归因于分子本身，而不是其最终的降解产物。
SummaryIsolated rat hearts were perfused by the recirculating Langendorff mode under normoxic conditions for 60 min. The Krebs-Ringer buffer was supplemented with 10mM glucose+12 IU/l insulin and either [U-14C]-fructose-1,6-bisphosphate (together with 5 mM cold fructose-1,6-bisphosphate) or [U-14C]-fructose (together with 5 mM cold fructose). At the end of perfusion, gaseous14CO2,14CO2 trapped in the perfusates,14C-lactate output and tissue14C-lactate were assayed in both groups of hearts. Analysis of high-energy compounds, glycogen, lactate, and pyruvate was also performed on the neutralized perchloric acid extracts of the freeze-clamped hearts. Data obtained from the14C catabolites, originating from the metabolism of the radiolabeled substrates, indicated that the isolated normoxic rat heart metabolizes an 8.5 times higher amount of fructose-1,6-bisphosphate (7.07 μmoles/min/g d. w.) than of fructose (0.83 μmoles/min/g d.w.). CrP, CrP/Cr, glycogen, and total lactate in both tissue and perfusate were significantly higher in fructose-1,6-bisphosphate-perfused hearts. The overall indication is that fructose-1,6-bisphosphate can be taken up in its intact form by myocytes and successively metabolized to support their energy demand, and that its effects on myocardial performance and metabolism should be attributed to the molecule itself rather than to its eventual degradation products.