Rats were made diabetic by the injection of streptozotocin on day 12 of pregnancy and were investigated on days 17 and 20 of pregnancy. A significant correlation between both maternal plasma triglyceride and nonesterified fatty acid levels with placental or fetal triglyceride content was found, although fetal weight did not change significantly. In order to investigate the source of the placental and fetal fat the rats received, intragastrically 24 h earlier, 1-14C-triolein (as a preformed fatty acid tracer) and tritiated water (as a marker of de novo fatty acid synthesis). Several maternal tissues, placenta, and fetuses were extracted and analysed for fatty acid radioactivity. Compared with non-diabetic pregnant rats, maternal 14C-label storage was reduced. In contrast, the placental and fetal tissues demonstrated a significant rise in 14C-label, similar in magnitude to the rise in their triglyceride content. The pattern of 3H incorporation also indicated a pronounced decrease in maternal fatty acid synthesis, but no increase in de novo fatty acid synthesis in the fetus or placenta. The findings show that fetal lipids in the pregnant rat originate both from maternal fatty acids and those synthesized in situ. The diabetes-induced increment in fetal triglyceride content is derived, however, from preformed maternal triglycerides or non-esterified fatty acids secondary to the increase in their concentration in the maternal circulation.
In 1957, Armstrong, McMillan and Shaw demonstrated a metabolite of epinephrine (E) and norepinephrine (NE) in normal human urine (2, 3). This substance, 3-methoxy,4-hydroxymandelic acid (VMA, for vanillylmandelic acid), was excreted in abnormally large amounts in three patients with pheochromocytomas (3). Recent studies of sympathomimetic amine metabolism (Figure 1) (4-7) suggested that the urinary excretion of the degradation products of E and NE, such as their 3-methylated derivatives (M and NM respectively) and VMA, might exceed E and NE excretion by some 10-or 20-fold. The diagnosis of pheochromocytoma might therefore be facilitated by analysis of urine for these phenolic compounds.Armstrong, Shaw and Wall's chromatographic technique for determination of urinary VMA (8, 9) was modified and used for the quantitative determination of VMA excretion in the urines of OH
Methods for the determination of urinary vanillylmandelic acid (VMA) have been reviewed and variations in VMA excretion in different disease states summarized. The determination of VMA excretion is believed to represent a reliable method for the detection of a pheochromocytoma. Colorimetric screening tests for the detection of elevated VMA excretion have been reviewed and evaluated as laboratory aids in the diagnosis of pheochromocytoma.
Pyruvate carboxylase (PC) activity was assayed in 27 chorionic villi samples
(CVS) obtained at 9-12 weeks of gestation. The kinetic properties of the CVS enzyme were
similar to those of liver PC; more than 7 5 % of PC activity was recovered in the mitochondrial
fraction of CVS. Apparent Km for pyruvate, ATP, acetyl CoA and HCO3 in the presence
of saturation concentrations of the other reactants, were 0.3, 0.44, 0.015 and 6.0 mmol/1,
respectively. The optimum pH was 7.5-8.0. The activity of PC in CVS was 3.2 ± 0.3
nmol/min/mg protein, which is severalfold higher than that of amniotic fluid fibroblasts.
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