Abstract
Abstract
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 × mg protein and controls (C) = 67.4 ± 3.9 nmole/min × mg protein; means ± SE, P 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 × mg protein vs 17.2 ± 0.5 nmole/min × mg protein, P 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.
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