Insulin, A Possible Regulator of Ketosis in Newborn and Suckling Rats

Insulin, A Possible Regulator of Ketosis in Newborn and Suckling Rats
复制标题

胰岛素,新生和乳鼠酮症的可能调节剂

DOI:
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发表时间:
1976
期刊:
影响因子:
3.6
通讯作者:
P. Zee
P. Zee
中科院分区:
医学3区
文献类型:
--
作者:
Y. Yeh;P. Zee

文献摘要

被引文献

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摘要:研究了胰岛素在新生大鼠和乳鼠酮症发生中可能的调节作用。出生时测得的总酮体平均血浆浓度为0.414 ± 0.037 μmol/ml。在出生后24小时内,酮的水平增加到初始值的4倍。在出生后的前5天内,血浆酮维持3至4倍的增加,但此后开始下降。新生大鼠出生时血浆胰岛素水平(62 ± 8 μU/ml)与喂养的成年大鼠血浆胰岛素水平(85 ± 10 μU/ml)相当。在出生后第一天,该水平降至28 μU/ml,并在整个哺乳期保持较低水平,尽管在接近断奶时有增加的趋势。乳鼠肝匀浆中酮生成能力与胰岛素水平呈负相关。胰岛素(0.125 mU/g体重,im)和葡萄糖(1.75 mg/g体重,ip)给药均抑制乳鼠血浆酮体。胰岛素给药增加了血浆胰岛素,但未能降低血糖。注射葡萄糖可增加血浆胰岛素和血糖。胰岛素和葡萄糖治疗均未改变血浆游离脂肪酸水平。这些数据表明,胰岛素的可用性有限,导致大鼠生酮率较高,从而诱导新生大鼠和哺乳大鼠出现酮病。推测:由母鼠哺乳的发育中大鼠的大部分能量来自牛奶中高脂肪和低碳水化合物含量。乳鼠体内的低浓度胰岛素不仅使胰岛素依赖性组织对葡萄糖的利用最小化,而且允许酮体的快速合成,然后酮体作为肝外组织(特别是脑)的能量来源。因此,可以满足乳鼠的能量需求,降低低血糖风险。进一步研究胰岛素在体外对脂肪分解、脂肪酸氧化和酮合成的影响,可以增加我们对胰岛素逆转乳鼠酮病作用的理解。
Extract: A possible regulatory role of insulin in the development of ketosis in newborn and suckling rats was inrestigated. The average plasma concentration of total ketone bodies measured at birth was 0.414 ± 0.037 μmol/ml. Within 24 hr after birth the level of ketones had increased to 4 times its initial value. The 3-to 4-fold increase in plasma ketones was maintained during the first 5 days of life but started to decline thereafter. Plasma insulin of newborn rats at birth (62 ± 8 μU/ml) was comparable to that of fed adult rats (85 ± 10 μU/ml). The levels decreased to 28 μU/ml on the first day of life and stayed low throughout the suckling period despite a tendency to increase at the time close to weaning. The capacities for ketone production in liver homogenates of suckling rats were inversely related to the levels of insulin. Administration of insulin (0.125 mU/g body weight, im) and glucose (1.75 mg/g body weight, ip) both suppressed plasma ketone bodies in suckling rats. Insulin administration increased plasma insulin but failed to decrease plasma glucose. Injection of glucose increased plasma insulin and glucose. Neither insulin nor glucose treatment changed the plasma levels of free fatty acids. These data suggest that a limited availability of insulin permits a high rat of ketogenesis and hence induced ketosis in newborn and suckling rats.Speculation: Developing rats suckled by their dams derive most of their energy from the high fat and low carbohydrate content of milk. The low concentration of insulin in suckling rats not only minimizes utilization of glucose by insulin-dependent tissues but permits a rapid synthesis of ketone bodies that then serve as energy sources for extrahepatic tissues, particularly the brain. Consequently, the energy requirements of suckling rats can be met with a reduced risk of hypoglycemia. Further studies on the effect of insulin on lipolysis, fatty acid oxidation, and ketone synthesis in vitro could add to our understanding of the action of insulin in reversing ketosis of suckling rats.