The rate of glucose turnover (R(a)) and gluconeogenesis (GNG) via pyruvate were quantified in seven full-term healthy babies between 24 and 48 h after birth and in twelve low-birth-weight infants on days 3 and 4 by use of [(13)C(6)]glucose and (2)H(2)O. The preterm babies were receiving parenteral alimentation of either glucose or glucose plus amino acid with or without lipids. The contribution of GNG to glucose production was measured by the appearance of (2)H on C-6 of glucose. Glucose R(a) in full-term babies was 30 +/- 1.7 (SD) micromol. kg(-1). min(-1). GNG via pyruvate contributed approximately 31% to glucose R(a). In preterm babies, the contribution of GNG to endogenous glucose R(a) was variable (range 6-60%). The highest contribution was in infants receiving low rates of exogenous glucose infusion. In an additional group of infants of normal and diabetic mothers, lactate turnover and its incorporation into glucose were measured within 4-24 h of birth by use of [(13)C(3)]lactate tracer. The rate of lactate turnover was 38 micromol. kg(-1). min(-1), and lactate C, not corrected for loss of tracer in the tricarboxylic acid cycle, contributed approximately 18% to glucose C. Lactate and glucose kinetics were similar in infants that were small for their gestational age and in normal infants or infants of diabetic mothers. These data show that gluconeogenesis is evident soon after birth in the newborn infant and that, even after a brief fast (5 h), GNG via pyruvate makes a significant contribution to glucose production in healthy full-term infants. These data may have important implications for the nutritional support of the healthy and sick newborn infant.
In a previous study, we demonstrated the complete dependence of the human fetus on the mother for its glucose needs. As alanine is considered the major glucogenic amino acid synthesized endogenously and an important source of urea nitrogen, in the present study we examined whether the human fetus at term gestation can produce alanine. 5 normal pregnant women, undergoing elective cesarean section, were given a constant infusion of [2,3-13C2]alanine in trace quantities for a period of 4 h prior to and during surgery. Isotopic steady state was achieved in the maternal blood by 1.5 h and maintained through anesthesia and surgery. The 13C enrichment (mol% excess) of alanine was measured in the peripheral blood of the mother and in the simultaneously obtained umbilical arterial and venous blood at delivery. Even though the umbilical venous and arterial concentrations of alanine were similar, a 42% decrease in 13C enrichment of alanine occurred between umbilical vein and artery, 1.00 ± 0.23 and 0.58 ± 0.15%, respectively (mean ± SD). These data suggest that the human fetus at term gestation following an overnight maternal fast produces alanine endogenously. This may serve to transfer nitrogen from fetal muscle to the liver for urea synthesis.
We studied 125~-insulin total and non-specific binding(1B) and 3~-deoxyglucose uptake (Gu) by 30d isolated fetal rabbit-brain cells (viability of >93%;n=8), to define the significance of the IR in the fetal brain. IB and Gu by brain cells were also assessed in the presence of lOmM phenylarsine oxide (PA) (n=4; prevents IR internalization) and 10vM chloroquin (CQ) (n=5; a lysosomotropic agent), to study the internalization and intracellular degradation of the IR (extracellular degradation was constant throughout the study). Peak specific IB per 6 . 4~1 0~ cells was achieved by 1-3 min (2.74+0.18%, X S E M ) , declining by 20 min (0.48+0.15;p<0.001). A decrease in the peak binding was observed with PA (0.40f0.08;p~0.001), whereas CQ resulted in a peak IB of 1.32+0.19, with no decline in IB at 20 min (2.11+0.49;p<0.01). 1x10=~11 insulin increased the Gu from 0.03+0.002to 0.05fP03nM/ 6 . 4~1 0~ cells (p<0.01). PA inhibited Gu and the insulin induced increase in Gu by the brain cells, while CQ inhibited the insulin induced increase in Gu alone (0.02+0.0007;p~0.01). Summary: 1)In the presence of PA, IB is decreased 2)CQ delayed the decline in peak IB secondary to its lysosomotropic effects and decreased intracellular IR degradation 2)Insulin augmented Gu by fetal brain cells 4)Inhibition of IR internalization by PA or lysosomotropic effects by CQ interfered with the insulin induced Gu by the brain cells. We conclude that the insulin induced Gu by fetal brain cells is associated with internalization of the IR. GALACTOSE-I-PHOSPHATE URIDYL TRANSFERASE SCREENING.1208 Chandradhar Dwivedi and Saburo Hara (Spon. by Festus 0. Adebonojo) D e p a r t m e n t -P e d i a t r i c s , Meharry Medical Coll ege, Nashvi 1 l e , TN. 37208Galactose-1-phosphate uridlytransferase (Gal-1-PUT) deficiency i s an inborn e r r o r of metabolism transmitted as an autosomal recessive t r a i t . Gal-1-PUT Screening was performed in a l l the newborns delivered a t Hubbard Hospital of Meharry Medical College f o r an e a r l y detection of t h i s deficiency. The appearance of fluorescent NADPH a f t e r incubating the blood spot with Gal-1-P, UOPG and NADP was used a s a screening t e s t . 2134 newborns were screened during May 1979-Sept. 1984. Three abnormal t e s t s were detected i n i t i a l y . After repeating the screening t e s t and quantitating the Gal-1-PUT, one case of t h i s deficiency was established. Two f a l s e positives were presumably due t o i n s u f f i c i e n t blood on the spot. This p a t i e n t i s a f u l l term f i r s t born male t o a Black mother. Gal-1-PUT was quantitated i n erythrocytes by UDPG consumption t e s t . The p a t i e n t had 1.6 u n i t s of a c t i v i t y , however, mother and her brother had 10.7 and 6.4 units respectively. U t i l i z a t i o n of one micromole of UDPG per gram hemoglobin per hour i s defined a s one u n i t . Patient was placed on modified galactose f r e e d i e t and successfully t r e a t e d . His growth and development a r e within normal l i m i t s f o r h i s age....
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