INCREASED GLUCOSE DEPENDENCE IN RESTING, IRON-DEFICIENT RATS
INCREASED GLUCOSE DEPENDENCE IN RESTING, IRON-DEFICIENT RATS
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DOI：
10.1152/ajpendo.1987.253.4.e461
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发表时间：
1987-10-01
影响因子：
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通讯作者：
DALLMAN, PR
中科院分区：
文献类型：
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作者：
BROOKS, GA;HENDERSON, SA;DALLMAN, PR
对静息缺铁和铁充足(对照)大鼠的血糖和乳酸周转率进行了评估，以验证缺铁会增加对葡萄糖代谢的依赖这一假设。21日龄雄性SD大鼠饲喂含铁6 mg/kg饲料(缺铁组)和含铁50 mg/kg饲料(补铁组)3~4wk。缺铁组变得贫血，血红蛋白水平为6.4.+-。0.2比13.8。+-。对照组为0.3g/dl。大鼠经颈静脉导管持续滴注D-[6-3H]葡萄糖和L-[U-14C]乳酸钠90min。从颈动脉导管采集一系列样本进行浓度和比活度测定。缺铁大鼠血糖显著升高(P<；0.05)。0.3比6.1.+-0.2 mm)和乳酸浓度(1.0.+-.0.1比0.8。+-。0.1毫米)。缺铁组有显著更高的葡萄糖周转率(67。+-。2对58+-。4.摩尔.cntdo.Kg-1.cntdo.Min-1)。在缺铁大鼠中，更多的14C(来自注入的[14C]-乳酸)被掺入到血糖中，这表明更多的代谢物回收。假设碳交叉校正系数为2，在缺乏的动物中，一半的血糖来自乳酸。相比之下，对照组只有25%的葡萄糖来自乳酸。缺乏的大鼠和对照组之间的乳酸周转率(不可逆处置)没有差异(191。+-。26比163。+-。15微克分子碳纳米点。Kg-1.cntdo.Min-1)w归因于14C循环。结果表明，缺铁大鼠对葡萄糖代谢的依赖程度更高。
Rates of blood glucose and lactate turnover were assessed in resting iron-deficient and iron-sufficient (control) rats to test the hypothesis that dependence on glucose metabolism is increased in iron deficiency. Male Sprague-Dawley rats, 21 days old, were fed a diet containing either 6 mg iron/kg feed (iron-deficient group) or 50 mg iron/kg feed (iron-sufficient group) for 3-4 wk. The iron-deficient group became anemic, with hemoglobin levels of 6.4 .+-. 0.2 compared with 13.8 .+-. 0.3 g/dl for controls. Rats received a 90-min primed continuous infusion of D-[6-3H]glucose and sodium L-[U-14C]lactate via a jugular catheter. Serial samples were taken from a carotid catheter for concentration and specific activity determinations. Iron-deficient rats had significantly (P < 0.05) higher blood glucose (7.1 .+-. 0.3 vs. 6.1 .+-. 0.2 mM) and lactate concentrations than controls (1.0 .+-. 0.1 vs. 0.8 .+-. 0.1 mM). The iron-deficient group had a significantly higher glucose turnover rate (67 .+-. 2 vs. 58 .+-. 4 .mu.mol .cntdot. kg-1 .cntdot. min-1) than the control group. Significantly more metabolite recycling in iron-deficient rats was indicated by greater incorporation of 14C (from infused [14C]-lactate) into blood glucose. Assuming a carbon crossover correction factor of 2, half of blood glucose arose from lactate in deficient animals. By comparison, only 25% of glucose arose from lactate in controls. Lack of a difference in lactate turnover (irreversible disposal) rates between deficient rats and controls (191 .+-. 26 vs. 163 .+-. 15 .mu.mol .cntdot. kg-1 .cntdot. min-1) ws attributed to 14C recycling. The results indicate a greater dependence on glucose metabolism in iron-deficient rats.