@entity6178 body metabolism during pregnancy in the XXXX .

@entity4876 @entity1522 @entity3952 @entity95 @entity653 @entity14992 @entity3929 @entity880 @entity6178 @entity1270 @entity3689 @entity1718
The aim of this study was to test the effect of lipid store mobilization on changes in @entity6178 body metabolism in pregnant @entity95 . Related blood parameters were studied in pregnant animals fed either ad libitum or submitted between days 21 of gestation and parturition first to 50% food restriction for 4 days and then to a complete fast. Ketogenesis from @entity3952 , @entity4876 and endogenous substrates was measured on days 0, 8, 18 and 28 of gestation in isolated liver cells prepared from females fasted for 48 h. In the does fed ad libitum, the concentration of non-esterified @entity1718 (NEFA) was higher than in non-pregnant animals and then increased about 2-fold in the last week before term. Total @entity6178 body concentrations increased slightly but significantly from day 27 until term. In the same period, glycemia decreased significantly. No variations were observed in @entity880 , @entity3929 and total @entity3689 concentrations. Food restriction on days 21 to 24 induced a quick rise in the plasma concentrations of NEFA, @entity6178 bodies and @entity653 . Further fasting resulted in the development of hyperketonemia which was more than 3 times that observed during prolonged fasting in non-pregnant @entity95 . There was no further increase in plasma NEFA level after day 27 of gestation. Food restriction and fasting decreased only the plasma level of total @entity1522 but had no significant effect on plasma concentrations of @entity880 and @entity3929 . In isolated liver cells, a marked and significant increase in the rate of ketogenesis from @entity3952 , @entity4876 and endogenous substrates was noted on day 28 of gestation in comparison with the preceding periods. It is concluded that @entity1270 was enhanced in late gestation, particularly with restricted feeding or in fasted animals; this enhancement was partly related to the increase of plasma NEFA concentrations and partly to the enhancement of hepatic ketogenesis in the mothers. The fact that the rate of hepatic ketogenesis was increased equally with @entity4876 and @entity3952 indicated that it could not be explained by a modification of @entity14992 transferase activity as @entity4876 directly crosses the mitochondrial membrane without using this pathway.
