IRON DEFICIENCY ANEMIA AND COMPENSATORY SNS ACTIVITY

铁缺乏和贫血的人和大鼠不能维持身体 冷压力时的温度。从现有的数据来看还不清楚 数据这种温度调节缺陷在多大程度上是次要的 与缺铁有关的贫血。交易所 输血大大改善了体温的维持， 促甲状腺激素(TSH)反应、甲状腺激素(T4)反应和三碘甲腺原氨酸(T3)反应 缺铁动物对冷应激的反应。高架 血浆和尿液去甲肾上腺素(NE)水平不受 这种纠正贫血的方法。关于代谢率的准确数据， 组织NE代谢、甲状腺激素代谢或实际 缺乏与贫血相关的生热活性。这个 这项提案的主要目标是界定 儿茶酚胺代谢导致体温调节降低 缺铁性贫血的能力。主要的假设是 试验表明，缺铁时SNS活性增加 对可能受损的甲状腺激素功能的代偿 (改编自大炮的型号)。有几个关键概念需要 在潜在影响之前确立为中间目标 对缺铁性贫血的生热作用进行了研究。首先： 是最小的代谢，最大的去甲肾上腺素刺激 ID和对照组大鼠的代谢率不同，并受 贫血?第二：静息代谢率的关系是什么 与对照组相比，ID中的温度？第三：IS 低智商时交感神经系统活动增加 温度呢？贫血的潜在过程 缺铁可能会影响生热作用 血流(微球)的量化以产热 器官，甲状腺激素向三碘甲状腺原氨酸(肝脏)的转化率 和棕色脂肪组织(5I-脱碘酶)，蝙蝠产热 活动(NE营业额和有丝分裂。对国内生产总值具有约束力)。准确的 记录IDA遗嘱中的代谢率和SNS活动 为理解温度调节提供了良好的基础 缺陷。未来的研究可能会检查可能的影响 组织铁缺乏对激素转换、受体部位的影响 调节、线粒体功能障碍和/或异常的中枢神经系统 生热作用的控制。

Iron deficient and anemic humans and rats fail to maintain body temperature when cold stressed. It is not clear from existing data how much of this thermoregulatory defect is secondary to the anemic associated with iron deficiency. Exchange transfusion acutely improves body temperature maintenance, (TSH) response, thyroxine (T4) response and triiodothyronine (T3) response of iron deficient animals to a cold stress. Elevated plasma and urine norepinephrine (NE) levels are unaffected by this correction of anemia. Accurate data on metabolic rate, tissue NE turnover, thyroid hormone metabolism or actual thermogenic activity relative to the anemia are lacking. The major goal of this proposal is to define the relationships of catecholamine metabolism to decreased thermoregulatory capacity in iron deficiency anemia. The major hypothesis being tested is that increased SNS activity in iron deficiency is compensatory to perhaps impaired thyroid hormone function (model adapted from Cannon). Several key concepts need to be established as intermediate goals before the underlying effects of iron deficiency anemia on thermogenesis are examined. First: Are the minimum metabolic, and the maximal NE stimulated metabolic rates different in ID and control rats and affected by anemia? Second: What is the resting metabolic rate relationship to temperature in ID compared to controls? Third: Is sympathetic nervous system activity increased in ID at low temperatures? The underlying processes whereby the anemia of iron deficiency may affect thermogenesis are examined by quantification of blood flow (microspheres) to thermogenic organs, rates of conversion of thyroxine to triiodothyronine (liver and brown adipose tissue (5I-deiodinase), BAT thermogenic activity (NE turnover and mito. GDP binding). The accurate documentation of metabolic rate and SNS activity in IDA will provide a good base for understanding the thermoregulatory defects. Future studies may then examine possible effects of tissue iron deficiency on hormone conversion, receptor site regulation, mitochondrial dysfunction, and/or abnormal CNS control of thermogenesis.