Heinze E, Vetter U
Diabetologia. 1987 Feb;30(2):100-3. doi: 10.1007/BF00274579.
For largely unknown reasons severe or moderate diabetes of pregnant rats results in pronounced fetal growth retardation. Therefore, some skeletal growth parameters of fetal rats from streptozotocin diabetic mothers were studied in vivo and in vitro. Two days post conception rats were intravenously injected with 65 mg/kg body weight streptozotocin. On day 20 post conception 8 normal and 8 diabetic rat mothers received 5 mu Ci 3-H thymidine intraperitoneally. One day later the experiments were terminated. Fetal body weight and body length were significantly (p less than 0.05-0.001) reduced in the hyperglycaemic rats compared to normal rats, as was the thymidine incorporation into rib cartilage (p less than 0.02). In the cell culture colony formation from isolated chondrocytes of normal and hyperglycaemic fetuses was determined. Proinsulin, insulin (62.5-250 ng/ml), insulin-like growth factor I and II (6.25-25 ng/ml) significantly (p less than 0.05-0.001) augmented colony formation in a dose-dependent manner, with the somatomedins being 8 times more effective than proinsulin or insulin. Isolated chondrocytes from hyperglycaemic compared to normal fetuses formed significantly (p less than 0.05-0.001) fewer colonies in the basal state and in response to all 4 hormones. The results confirm the growth retardation of fetuses from diabetic rat mothers. A reduced responsiveness of chondrocytes from hyperglycaemic fetuses to various growth factors could be demonstrated as compared to cells from normal fetuses.
由于 largely unknown reasons 严重或中度妊娠大鼠糖尿病会导致明显的胎儿生长迟缓。因此,对链脲佐菌素诱导糖尿病母亲所生胎鼠的一些骨骼生长参数进行了体内和体外研究。受孕后两天,大鼠静脉注射 65 mg/kg 体重的链脲佐菌素。受孕后第 20 天,8 只正常和 8 只糖尿病大鼠母亲腹腔注射 5 μCi 3-H 胸腺嘧啶核苷。一天后实验结束。与正常大鼠相比,高血糖大鼠的胎儿体重和体长显著降低(p < 0.05 - 0.001),胸腺嘧啶核苷掺入肋软骨的量也显著降低(p < 0.02)。在细胞培养中,测定了正常和高血糖胎儿分离软骨细胞的集落形成。胰岛素原、胰岛素(62.5 - 250 ng/ml)、胰岛素样生长因子 I 和 II(6.25 - 25 ng/ml)以剂量依赖方式显著增加集落形成(p < 0.05 - 0.001),生长调节素的效力比胰岛素原或胰岛素高 8 倍。与正常胎儿相比,高血糖胎儿分离的软骨细胞在基础状态下以及对所有 4 种激素的反应中形成的集落显著减少(p < 0.05 - 0.001)。结果证实了糖尿病大鼠母亲所生胎儿的生长迟缓。与正常胎儿的细胞相比,高血糖胎儿软骨细胞对各种生长因子的反应性降低。