Effects of exogenous hormones and glucose on plasma levels and hepatic metabolism of amino acids in the fetus and in the newborn rat

Girard, Jean; I, Guillet; Marty, Jean-Claude; Assan, R; Eb, Marliss

doi:10.1007/bf00420976

Cited by 30 publications

(19 citation statements)

References 39 publications

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“…These decreases were statistically significant for glutamic acid, citrulline, alanine, valine, the sum of the branched chain group, and the total of all 19 amino acids quantitated. Fetal amino acid concentrations were approximately 2-fold higher than maternal values in control animals and, for the most part, corresponded closely with those previously reported by Girard et al (14) for full-term fetal rats.…”

Section: Resultssupporting

confidence: 90%

Protein Turnover in Tissues of the Rat Fetus following Maternal Starvation

et al. 1986

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ABSTRACT. The effects of maternal starvation upon protein turnover in various tissues of the fetal rat were determined. Protein synthesis was determined in fetal tissues by the intravenous injection of "massive" amounts of 3H-phenylalanine into the maternal circulation, followed by measurements of tissue free and protein-bound phe specific radioactivity in fetal diaphragm, heart, liver, and brain. Rates of protein degradation in fetal tissues were assessed by subtracting protein accretion rates from protein synthesis. Fractional rates of protein synthesis were minimally affected by maternal starvation in diaphragm, heart, and brain. The major factor contributing to reduced fetal protein accretion in these fetal tissues during maternal starvation was enhanced protein breakdown. These findings differ from those previously reported in young adult rodents following fasting or malnutrition. The rapid accretion of protein during growth of the fetus represents a balance between rates of protein synthesis and protein degradation. We have previously reported (l,2) that rates of protein accretion in various tissues/orl 1s of the fetal rat at different stages of gestation result from alterations in both rates of protein synthesis and breakdown. Thus, in both diaphragm and heart, protein accretion during the most rapid phase of fetal growth is accomplished by higher rates of synthesis and lower rates of degradation when compared to a time of lesser growth (1).It is, therefore, obvious that perturbations in fetal growth may result from alterations in either of these two components of protein turnover. Very few studies have addressed the mechanism(~) of altered fetal growth in these terms. We have determined protein turnover in vivo in various tissues of the fetal rat following total caloric restriction of maternal rats for a 72-h period between 18-2 1 days gestation. Our results indicate that enhanced protein degradation is a critically important determinant of reduced rates of protein accretion in fetal diaphragm, heart, and brain following maternal starvation. METHODSAnimals. Virgin Sprague-Dawley rats were mated at 100 days of age. Day 0 of gestation was defined as the day on which a pan plug was found (3). Throughout the mating period and the subsequent gestational period, animals were kept in a room controlled at 22 a 1" C with a 12-h on-off light cycle. Control animals were fed Wayne Lab Blox (Allied Mills, Chicago, IL, 24% protein) ad libitum throughout gestation. Animals in the experimental group were fed the same diet until day 18 of gestation, after which they were provided only with water.Determination of protein synthesis. We utilized the method of Garlick et al. (4) to determine protein synthesis in vivo. With this technique, "massive" amounts of 3H-phe are injected into animals in an attempt to flood the precursor pools of protein synthesis. The precursor pool specific radioactivity is maintained relatively constant during the time period over which incorporation of 3H-phe into protein is measured. The applica...

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Section: Resultssupporting

confidence: 90%

Protein Turnover in Tissues of the Rat Fetus following Maternal Starvation

et al. 1986

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“…Atomique, Saclay, France) 16 hr after birth and blood was sampled.30 min later as described previously (18,19).…”

Section: Methodsmentioning

confidence: 99%

“…The technique for blood sampling and the biochemical methods used for metabolite, amino acid, and hormone determinations were as described previously (17)(18)(19). Enzymatic techniques were used for the determination of lactate (38), pyruvate (39), glycerol (49), alanine (50), 3-hydroxybutyrate (33), acetoacetate (34), and glucose (2) on blood perchloric acid filtrates.…”

Section: Methodsmentioning

confidence: 99%

“…Measurement of gluconeogenic rate in vivo was performed as described previously (12,18,19) using lactate space equal to the total body water, i.e., 80 mg/100 g body wt, and glucose and alanine spaces equal to the extracellular water, Le., 60 m1/100 g body wt. The validity of this method has been discussed previously (18,19).…”

Section: Methodsmentioning

confidence: 99%

“…The validity of this method has been discussed previously (18,19). The separation of labeled glucose and charged compounds was performed using ion-exchange resins as described previously (1 2).…”

Section: Methodsmentioning

confidence: 99%

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Influence of Exogenous Cortisol and Triglyceride Feeding on Glucose Homeostasis in the Fasted Newborn Rat

et al. 1978

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SummaryThe effects of cortisol injection (0.2 mg/g body wt) at birth and of triglyceride feeding (20 mg/g body wt) 13 hr after birth have been studied in 16hr-old fasted newborn rats. Cortisol produced a 10% decrease in body weight and in protein concentrations of carcass, hindlimb muscle, and liver. Furthermore, cortisol induced a 60% fall in carcass lipid levels. Cortisol caused a 2-fold increase in fasting blood glucose level. This effect resulted from a stimulation of gluconeogenesis (as shown by the 2-to 3-fold rise in the rate of conversion of labeled lactate or alanine to glucose). Several factors influenced this response: 1) increase in circulating gluconeogenic substrates (lactate, pyruvate, alanine,' proline, and glutamine), 2) increase in plasma glucagon, 3) a small rise in plasma free fatty acids (FFA) arising from the catabolism of endogenous lipids, thereby providing additional energy for the hepatic conversion of gluconeogenic substrates to glucose. A concurrent decrease in.glucose utilization was unlikely since: 1) the rate of glucose disappearance after an ip glucose load was similar in fasted and cortisol-treated newborns, and 2) the rise in plasma insulin occurring after cortisol injection would ordinarily tend to increase glucose utilization.Triglyceride feeding was associated with a Zfold rise in fasting blood glucose. This effect was secondary to a stimulation of gluconeogenesis by provision of free FFA, as demonstrated by the 2.5-fold increase in the conversion in vivo of labeled lactate and alanine into glucose.In newborn rats injected with cortisol, the levels of both plasma FFA and blood ketone bodies remained far below those in suckling newborns of the same age. The combination of cortisol injection at birth with triglyceride feeding 13 hr after birth caused a Sfold increase in blood glucose levels in the ldhr-old newborn rats. The stimulating effects of cortisol on gluconeogenesis were potentiated by triglyceride feeding, as shown by the 3-to 4-fold increase in the rate of lactate or alanine conversion to glucose. However, cortisol markedly decreased the ketosis induced by triglyceride feeding and increased plasma triglycerides. SpeculationCorticosteroids have been used in the treatment of symptomatic hypoglycemia in newborn infants. In fasted newborn rats, cortisol partially prevents hypoglycemia, but at the cost of increased protein catabolism. Moreover, cortisol has an antiketogenic effect, thus decreasing the availability of ketones as alternate fuel for brain metabolism and as Drecursor for brain l i~i d svnthesis. If such data can be extrapolated to the human newborn, the prolonged use of corticosteroids in the treatment of neonatal hypoglycemia seems less physiologic than adequate parenteral energy substrate provision in the form of intralipid and gluconeogenic precursors (lactate, amino acids, and glycerol).Profound hypoglycemia has been shown to occur in newborn rats after a fast of 16-24 hr beginning at birth (5,17,19). This hypoglycemia resulted from an inadequate rate of g...

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