Control of fetal and neonatal glucose metabolism by pancreatic hormones

Girard, Jean

doi:10.1016/s0950-351x(89)80055-2

Cited by 15 publications

(23 citation statements)

References 98 publications

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“…1981], Hormonal Changes at Birth Immediately after birth, there is a tran sient neonatal hypoglycemia and an increase in plasma glucagon and catecholamines and a fall in plasma insulin in newborn rats delivered by cesarean section and main tained at 37 °C ( fig. 3) [Girard et al, 1973: Padburyand Martinez, 1988Girard, 1989], As the changes in pancreatic hormone secre tion occur in the absence of hypoglycemia in newborn rats delivered vaginally and kept with their mother at 30 °C [Kervran et al, 1976] or in newborn rats delivered by cesar ean section and exposed at 24 °C [Blazquez et al, 1974], it has been suggested that the changes in plasma insulin and glucagon re sulted from an increase activity of sympa thetic nervous system due to stress of birth (hypoxia during delivery, cold exposure, cord cutting etc.) [Girard, 1989].…”

Section: Supply O F Carbohydrate From the Milkmentioning

confidence: 99%

“…3) [Girard et al, 1973: Padburyand Martinez, 1988Girard, 1989], As the changes in pancreatic hormone secre tion occur in the absence of hypoglycemia in newborn rats delivered vaginally and kept with their mother at 30 °C [Kervran et al, 1976] or in newborn rats delivered by cesar ean section and exposed at 24 °C [Blazquez et al, 1974], it has been suggested that the changes in plasma insulin and glucagon re sulted from an increase activity of sympa thetic nervous system due to stress of birth (hypoxia during delivery, cold exposure, cord cutting etc.) [Girard, 1989]. Indeed, hypoxia or catecholamine infusion in the fetus in utero markedly stimulates glucagon secretion and inhibits insulin secretion, and cord cutting triggers glucagon secretion and inhibits insulin secretion in the neonate [Gi rard and Sperling.…”

Section: Supply O F Carbohydrate From the Milkmentioning

confidence: 99%

“…Injections o gluca gon, epinephrine and norepinephrine into the rat fetus in utero have induced the ap pearance of liver PEPCK prematurely, while injection of insulin into the newborn rat at delivery markedly impaired the postnatal in crease in liver PEPCK [Review in Girard, 1989], More recently, it has been shown that injection of glucagon or cAMP to fetal rats in utero caused a marked induction of mRNA for PEPCK [Garcia-Ruiz et al. 1978;Cimbala et al, 1982], thus strongly suggesting that cAMP regulates PEPCK synthesis at the transcriptional level.…”

Section: Hormonal Control O F the Development O F Hepatic Gluconeogenmentioning

confidence: 99%

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Metabolic Adaptations to Change of Nutrition at Birth

Girard

1990

Neonatology

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118

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Birth represents a dramatic change of nutrition from a fetal diet rich in carbohydrates and poor in fat to a neonatal diet rich in fat and poor in carbohydrates. Gluconeogenesis and ketogenesis are absent or very low in the fetal liver when the mother is correctly fed, and these metabolic pathways emerge after birth to reach adult values after 24 h. Gluconeogenesis increases rapidly in the liver of the newborn in parallel with the appearance of phosphoenolpyruvate carboxykinase (PEPCK), the rate-limiting enzyme of this metabolic pathway. The rise in plasma glucagon, the fall in plasma insulin and the resulting increase in liver cAMP which occur immediately after birth are the factors which induce the activation of liver PEPCK gene transcription. The appearance of ketogenesis is also controlled by the changes of plasma insulin and glucagon that increase the capacity for liver fatty acid oxidation by decreasing lipogenesis and malonyl-CoA concentration, by reducing the sensitivity of carnitine palmitoyl-CoA I to the inhibitory influence of malonyl-CoA, and by activating hydroxymethylglutaryl-CoA synthase by desuccinylation. Once liver PEPCK has reached adult value, i.e. 12 h after birth, other factors are involved in the regulation of hepatic gluconeogenesis. Indeed, the supply of gluconeogenic substrates and of free fatty acid is of crucial importance to support a high rate of gluconeogenesis and to maintain normoglycemia in the newborn. In the liver, fatty acid oxidation provides essential co-factors (acetyl-CoA, NADH and ATP) to support gluconeogenesis, and in peripheral tissue fatty acid oxidation inhibits glucose oxidation and stimulates the production of gluconeogenic precursors (lactate, pyruvate and alanine). Similar mechanisms are operative in human newborn. A defective hepatic fatty acid oxidation is likely to explain the frequent hypoglycemia observed in small-for-date neonates. Administration of oral triglycerides is an efficient mean to prevent hypoglycemia in these newborns.

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Section: Supply O F Carbohydrate From the Milkmentioning

confidence: 99%

Section: Supply O F Carbohydrate From the Milkmentioning

confidence: 99%

Section: Hormonal Control O F the Development O F Hepatic Gluconeogenmentioning

confidence: 99%

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Metabolic Adaptations to Change of Nutrition at Birth

Girard

1990

Neonatology

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118

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“…The metabolic similarities in energy stor age and utilization present in the neonatal guinea pig and the human infant support the use of the guinea pig as a model for research on neonatal carbohydrate metabolism and the major role of galactose in this metabolism [9,[28][29][30][31][32], Galactose metabolism may have its greatest impact during the first few days of life, as suggested by the peak in galactose-1-phosphate uridyltransferase activity. Given a constant galactose load, serum concentrations of galactose have been shown to increase after 7 days in the human infant, suggesting de creased hepatic uptake [33].…”

Section: Discussionmentioning

confidence: 99%

The Neonatal Guinea Pig as a Model for Human Galactose Metabolism: Galactose-1-Phosphate Uridyltransferase Activity

Lundell¹,

Savaiano²

1993

Neonatology

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The specific activity of galactose-1-phosphate uridyltransferase was measured in fetal and neonatal guinea pig liver during the first 10 days of age. Activity was approximately six times greater than in adult animals, and peaked during the first 48 h after birth. Activity dropped sharply during the next 2 days, followed by a gradual decline. Liver galactose and glycogen levels were stable throughout the study period. Liver glucose rose significantly after birth, then dropped slightly. The pattern of uridyltransferase in the guinea pig is similar to that reported for phosphoenolpyruvate carboxylkinase and pyruvate carboxylase. Compared to the rat, specific activity of uridyltransferase peaked earlier, possibly due to the guinea pig’s advanced maturity.

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“…[13][14][15][16] have been selected: neural energy supply, glucose competition, and the provision of ketones as neural fuel.…”

Section: Prevention and Management Of Neonatal Hypoglycaemia Anil Mehtamentioning

confidence: 99%