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低血糖:对胚胎而言,多低才算过高?

Hypoglycemia: how little is too much for the embryo?

作者信息

Sadler T W, Hunter E S

出版信息

Am J Obstet Gynecol. 1987 Jul;157(1):190-3. doi: 10.1016/s0002-9378(87)80378-2.

DOI:10.1016/s0002-9378(87)80378-2
PMID:3605253
Abstract

The effects of hypoglycemia on mammalian embryos undergoing neurulation (third to fourth week of human development) were investigated. Mouse embryos were maintained for 28 hours in whole embryo culture in serum collected from rats that had received 50 units of 100 United States Pharmacopeia insulin units per milliliter. Glucose concentrations used were 40, 60, 80, and 147 mg/dl (normal blood glucose in the pregnant mouse is 125 mg/dl). After the culture period embryos were evaluated for malformations and growth and compared with those maintained under euglycemic conditions. The results demonstrate that glucose concentrations approximately 50% of normal maternal levels were teratogenic but not growth inhibitory, whereas concentrations in the range of 30% to 40% of maternal levels were lethal to the embryo. Furthermore, a 14-hour exposure to reduced blood sugar in either the first or second half of the culture period produced malformations.

摘要

研究了低血糖对处于神经胚形成阶段(人类发育的第三至第四周)的哺乳动物胚胎的影响。将小鼠胚胎在从接受每毫升含50单位100美国药典胰岛素单位的大鼠采集的血清中进行全胚胎培养28小时。使用的葡萄糖浓度分别为40、60、80和147毫克/分升(怀孕小鼠的正常血糖为125毫克/分升)。培养期结束后,对胚胎进行畸形和生长评估,并与在正常血糖条件下培养的胚胎进行比较。结果表明,约为正常母体水平50%的葡萄糖浓度具有致畸性但不抑制生长,而在母体水平30%至40%范围内的浓度对胚胎是致命的。此外,在培养期的前半段或后半段,胚胎暴露于低血糖环境14小时会导致畸形。

相似文献

1
Hypoglycemia: how little is too much for the embryo?低血糖:对胚胎而言,多低才算过高?
Am J Obstet Gynecol. 1987 Jul;157(1):190-3. doi: 10.1016/s0002-9378(87)80378-2.
2
Embryopathic effects of short-term exposure to hypoglycemia in mouse embryos in vitro.
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Effects of maternal diabetes on embryogenesis.母体糖尿病对胚胎发育的影响。
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Lack of teratogenic effect of brief maternal insulin-induced hypoglycemia in rats during late neurulation.孕鼠在神经胚形成后期短暂胰岛素诱导的低血糖对大鼠无致畸作用。
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Development of rat embryos in culture media containing different concentrations of normal and diabetic rat serum.在含有不同浓度正常和糖尿病大鼠血清的培养基中大鼠胚胎的发育情况。
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Evidence for multifactorial origin of diabetes-induced embryopathies.糖尿病诱导胚胎病多因素起源的证据。
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Fuel-mediated teratogenesis: biochemical effects of hypoglycemia during neurulation in mouse embryos in vitro.
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引用本文的文献

1
Effects of alpha-lipoic acid supplementation on maternal diabetes-induced growth retardation and congenital anomalies in rat fetuses.补充α-硫辛酸对母体糖尿病诱导的大鼠胎儿生长迟缓及先天性异常的影响。
Mol Cell Biochem. 2004 Jun;261(1-2):123-35. doi: 10.1023/b:mcbi.0000028747.92084.42.
2
Embryonic growth impaired by maternal hypoglycemia during early organogenesis in normal and diabetic rats.正常和糖尿病大鼠在器官发生早期,母体低血糖会损害胚胎发育。
Acta Diabetol. 1994 Sep;31(3):141-6. doi: 10.1007/BF00570368.
3
The fetus of the diabetic mother: growth and malformations.
糖尿病母亲的胎儿:生长与畸形
Arch Dis Child. 1988 Oct;63(10 Spec No):1119-21. doi: 10.1136/adc.63.10_spec_no.1119.
4
Abnormal ambient glucose levels inhibit proteoglycan core protein gene expression and reduce proteoglycan accumulation during chondrogenesis: possible mechanism for teratogenic effects of maternal diabetes.异常的环境葡萄糖水平会抑制蛋白聚糖核心蛋白基因的表达,并减少软骨形成过程中蛋白聚糖的积累:这可能是母体糖尿病致畸作用的机制。
Proc Natl Acad Sci U S A. 1989 Dec;86(24):10113-7. doi: 10.1073/pnas.86.24.10113.
5
Effects of hyperglycaemia on sorbitol and myo-inositol contents of cultured embryos: treatment with aldose reductase inhibitor and myo-inositol supplementation.高血糖对培养胚胎中山梨醇和肌醇含量的影响:用醛糖还原酶抑制剂治疗及补充肌醇
Diabetologia. 1990 Oct;33(10):597-602. doi: 10.1007/BF00400203.