Wapnir R A, Stiel L
Proc Soc Exp Biol Med. 1985 Apr;178(4):546-50. doi: 10.3181/00379727-178-42040.
Maternal lipemia (L), one of the consequences of poorly controlled diabetes in gestation, was induced in pregnant rats by feedings of a diet containing 45% fat. The maternal condition was associated with fetal L and moderate ketonemia. L fetuses had an elevated liver glycerol kinase (EC 2.7.1.30), when assayed 1 day before term (L = 82.5 +/- 3.8 nmole/min X mg protein and controls (C) = 67.4 +/- 3.9 nmole/min X mg protein; means +/- SE, P less than 0.01). However, neither hepatic cytosolic glycerophosphate (GcPO4) dehydrogenase (EC 1.1.1.94) nor mitochondrial GcPO4 oxidase (EC 1.1.99.5) were altered. GcPO4 oxidase was lower in the striated muscle of L than in that of C fetuses (13.7 +/- 1.2 nmole/min X mg protein vs 17.2 +/- 0.5 nmole/min X mg protein, P less than 0.05). The results of the present study suggest that L, in utero, may cause an alteration in overall glycerol oxidative capacity in liver and GcPO4 in muscle. These changes appear to be compatible with a shift in the capacity of L fetuses to handle glycerol which may relate to postnatal fuel utilization by L offspring.
母体脂血（L）是妊娠期糖尿病控制不佳的后果之一，通过喂食含45%脂肪的饲料在怀孕大鼠中诱发。母体状况与胎儿脂血和中度酮血症相关。在足月前1天检测时，脂血胎儿的肝脏甘油激酶（EC 2.7.1.30）活性升高（L = 82.5±3.8纳摩尔/分钟×毫克蛋白，对照组（C） = 67.4±3.9纳摩尔/分钟×毫克蛋白；均值±标准误，P＜0.01）。然而，肝胞质甘油磷酸（GcPO4）脱氢酶（EC 1.1.1.94）和线粒体GcPO4氧化酶（EC 1.1.99.5）均未改变。脂血胎儿横纹肌中的GcPO4氧化酶低于对照组胎儿（13.7±1.2纳摩尔/分钟×毫克蛋白对17.2±0.5纳摩尔/分钟×毫克蛋白，P＜0.05）。本研究结果表明，子宫内的脂血可能会导致肝脏整体甘油氧化能力和肌肉中GcPO4的改变。这些变化似乎与脂血胎儿处理甘油能力的转变相一致，这可能与脂血后代出生后的燃料利用有关。
