Gewolb I H, Rooney S A, Barrett C, Ingleson L D, Light D, Wilson C M, Walker Smith G J, Gross I, Warshaw J B
Exp Lung Res. 1985;8(2-3):141-51. doi: 10.3109/01902148509057518.
Pulmonary maturation was studied in fetuses in streptozotocin-diabetic rats on the final four days of gestation. Diabetes was induced prior to conception by the intravenous injection of streptozotocin. Fetuses were hyperglycemic but did not manifest hyperinsulinemia. Whole lung total phospholipid, phosphatidylcholine, and disaturated phosphatidylcholine were significantly decreased in the diabetic group on day 21 (term = 22 days), but not prior to or after that point in gestation. Morphologic analysis also revealed a decreased number of type II cells and lamellar bodies per alveolar lining cell in the diabetic group only on day 21, coincident with the changes in phospholipid analysis. Activities of enzymes involved in fetal pulmonary phospholipid synthesis were measured to see if differences could account for the observed developmental delay. No significant differences between diabetic and control lungs were noted in any of the enzymes studied from days 20-22, with the exception of an increase in cholinephosphate cytidylyltransferase activity in the diabetic fetuses on day 22. Immaturity in both biochemical and morphologic indices of lung development was present at a specific time late in the diabetic rat gestation. This maturational delay could not be accounted for by changes in the activities of enzymes involved in phospholipid synthesis. The fetus of the streptozotocin-diabetic rat provides a useful model to study the effects of hyperglycemia on fetal lung development.
在妊娠最后四天，对链脲佐菌素诱导糖尿病大鼠的胎儿进行肺成熟度研究。在受孕前通过静脉注射链脲佐菌素诱导糖尿病。胎儿血糖升高，但未表现出高胰岛素血症。糖尿病组在第21天（足月为22天）时，全肺总磷脂、磷脂酰胆碱和二饱和磷脂酰胆碱显著降低，但在妊娠该时间点之前或之后未出现这种情况。形态学分析还显示，仅在第21天，糖尿病组每个肺泡衬里细胞中的II型细胞和板层小体数量减少，这与磷脂分析的变化一致。测量参与胎儿肺磷脂合成的酶的活性，以观察差异是否能解释观察到的发育延迟。在第20 - 22天研究的任何一种酶中，糖尿病组和对照组肺之间均未发现显著差异，但糖尿病胎儿在第22天的胆碱磷酸胞苷转移酶活性有所增加。糖尿病大鼠妊娠后期的特定时间出现了肺发育的生化和形态学指标不成熟的情况。这种成熟延迟不能用参与磷脂合成的酶的活性变化来解释。链脲佐菌素诱导糖尿病大鼠的胎儿为研究高血糖对胎儿肺发育的影响提供了一个有用的模型。
