Insulin and Glucagon during the Perinatal Period: Secretion and Metabolic Effects on the Liver

Ktorza, Alain; Bihoreau, Marie-Thérèse; Nurjhan, Nurjahan; Picon, L; Girard, Jean

doi:10.1159/000242173

Cited by 70 publications

(34 citation statements)

References 84 publications

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“…According to its magnitude, gestational hyperglycemia had quite different effects on plasma insulin concentrations in the newborns. Compared with controls, newborns from SH rats developed marked hyperinsulinemia, in agreement with many other reports demonstrating hyperinsulinemia in full-term fetuses from either mildly diabetic mothers (reviewed in 14) or slightly hyperglycemic mothers (7,17). By contrast, high gestational hyperglycemia failed to increase plasma insulin concentration in the newborn rats.…”

Section: Discussionsupporting

confidence: 91%

Impaired Hepatic Glycogenolysis Related to Hyperinsulinemia in Newborns from Hyperglycemic Pregnant Rats

et al. 1990

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ABSTRACT. We have investigated the respective roles of insulin and glucagon in the initiation of hepatic glycogen degradation during the early postnatal period in rats, with special regard on the inhibitory effect of insulin on this process. Pregnant rats were rendered either slightly (8.5 mM) or highly hyperglycemic (22 mM) by infusing glucose during the last week of pregnancy. Fasted, newborn rats were studied from delivery to 16 h postpartum. At birth, newborns from slightly hyperglycemic rats showed higher glvcemia and insulinemia and lower plasma glucagonemia --compared with controls. Newborns from highly hyperglycemic rats were still more hyperglycemic and exhibited low plasma glucagon concentrations, but they were not hyperinsulinemic. In control newborns, hepatic glycogen breakdown was triggered by 2 h after delivery. By contrast, hyperglycemic-hyperinsulinemic newborns (newborns from slightly hyperglycemic rats) were unable to mobilize liver glycogen before 8-10 h after delivery. In hyperglycemicnormoinsulinemic newborns (newborns from highly hyperglycemic rats), hepatic glycogen concentration significantly started to decline 2 h after delivery and was no longer different from controls at 8 h. Anti-insulin serum injection at delivery promoted a prompt decrease in liver glycogen stores in controls as well as in newborns from slightly hyperglycemic rats. Phosphorylase alsynthase a ratio rose rapidly after delivery in controls and in newborns from highly hyperglycemic rats (maximum 4 h), whereas in newborns from slightly hyperglycemic rats, it rose much more slowly than in the two other groups (maximum 16 h). These data suggest that, in newborns from hyperglycemic mothers, hyperinsulinemia during late fetal and early neonatal life is the main factor preventing postnatal hepatic glycogenolysis. glucose homeostasis in newborn mammals. The breakdown of the large glycogen stores that have been accumulated in the fetal liver during late pregnancy represents the more rapidly available endogenous source of glucose (1, 2).Hepatic glycogen metabolism is primarily controlled by the respective concentrations of insulin and glucagon in the plasma (3), and it could be assumed that even a slight change in the secretion of one or both hormones during the fetal life may hamper the metabolic adaptation of the newborn to extrauterine life. This is suggested by the situation of infants of poorly controlled diabetic women in whom the severe postnatal hypoglycemia is mainly due to defective glucose production (4).We have previously shown that newborn rats of dams rendered slightly hyperglycemic by continuous glucose infusion during the last third of pregnancy were hyperglycemic at birth, but were profoundly hypoglycemic in the early postnatal period. This hypoglycemia seemed to be due, in a major part, to a defective postnatal hepatic glycogen breakdown, in contrast to control newborns, which exhibited sustained postnatal hepatic glycogenolysis (5). Concurrently, in newborns from hyperglycemic rats, the insulin/glucagon molar ...

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Section: Discussionsupporting

confidence: 91%

Impaired Hepatic Glycogenolysis Related to Hyperinsulinemia in Newborns from Hyperglycemic Pregnant Rats

et al. 1990

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Section: Glucose Homeostasis and Fetal Nutritionmentioning

confidence: 99%

Hyperinsulinism in Infancy: From Basic Science to Clinical Disease

Dunne

Cosgrove²,

Shepherd³

et al. 2004

Physiological Reviews

263

277

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Dunne, Mark J., Karen E. Cosgrove, Ruth M. Shepherd, Albert Aynsley-Green, and Keith J. Lindley. Hyperinsulinism in Infancy: From Basic Science to Clinical Disease. Physiol Rev 84: 239–275, 2004; 10.1152/physrev.00022.2003.—Ion channelopathies have now been described in many well-characterized cell types including neurons, myocytes, epithelial cells, and endocrine cells. However, in only a few cases has the relationship between altered ion channel function, cell biology, and clinical disease been defined. Hyperinsulinism in infancy (HI) is a rare, potentially lethal condition of the newborn and early childhood. The causes of HI are varied and numerous, but in almost all cases they share a common target protein, the ATP-sensitive K+ channel. From gene defects in ion channel subunits to defects in β-cell metabolism and anaplerosis, this review describes the relationship between pathogenesis and clinical medicine. Until recently, HI was generally considered an orphan disease, but as parallel defects in ion channels, enzymes, and metabolic pathways also give rise to diabetes and impaired insulin release, the HI paradigm has wider implications for more common disorders of the endocrine pancreas and the molecular physiology of ion transport.

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Section: Foetal Glycogen Synthesis and Foetal Glycogenolysismentioning

confidence: 99%

“…The endocrine events believed to trigger neonatal glucose production and the mobilization of fat from peripheral stores include increased epinephrine secretion and a rapid fall in the insulin to glucagon ratio, as occurs during the first few hours of life. This change is accounted for by both a fall in the plasma insulin concentration and a surge in the plasma glucagon concentration that occur at this time (Ktorza et al, 1985). The neonate defends itself against hypoglycaemia by decreasing insulin production and simultaneously increasing secretions of glucagon, epinephrine, growth hormone and cortisol, hormones that work together in a counter-regulatory function that counteracts the effect of insulin and thus causes increased hepatic glucose output by other means, initially from insulin and decreased glucagon (Sunehag and Haymond, 2002).…”

Section: Neonatal Glycogenolysismentioning

confidence: 99%

Foetal and neonatal energy metabolism in pigs and humans: a review

Mota-Rojas¹,

Orozco-Gregorio²,

Villanueva-García³

et al. 2011

Vet. Med. - Czech

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ABSTRACT:The aim of this review was to elaborate a conceptual framework of the most important aspects of the main biochemical processes of synthesis and breakdown of energy substrates that human and pig foetuses and newborns can use during the transition from foetus to newborn. Under normal physiological conditions, the growth and development of the foetus depends upon nutrients such as glucose, lipids and amino acids. In addition to the maternal and foetal status, genetic factors are also reported to play a role. The main function of the placenta in all species is to promote the selective transport of nutrients and waste products between mother and foetus. This transport is facilitated by the close proximity of the maternal and foetal vascular systems in the placenta. The foetus depends on the placental supply of nutrients, which regulates energy reserves by means of glycogen storage. Also, the synthesis of foetal hepatic glycogen guarantees energy reserves during perinatal asphyxia or maternal hypoglycaemia. However, the foetus can also obtain energy from other resources, such as gluconeogenesis from the intermediary metabolism of the Krebs cycle and most amino acids. Later, when the placental glucose contribution ends during the transition to the postnatal period, the maturation of biological systems and essential metabolic adaptations for survival and growth is required. The maintenance of normoglycaemia depends on the conditions that determine nutrient status throughout life: the adequacy of glycogen stores, the maturation of the glycogenolytic and gluconeogenic pathway, and an integrated endocrine response.

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Insulin and Glucagon during the Perinatal Period: Secretion and Metabolic Effects on the Liver

Cited by 70 publications

References 84 publications

Impaired Hepatic Glycogenolysis Related to Hyperinsulinemia in Newborns from Hyperglycemic Pregnant Rats

Impaired Hepatic Glycogenolysis Related to Hyperinsulinemia in Newborns from Hyperglycemic Pregnant Rats

Hyperinsulinism in Infancy: From Basic Science to Clinical Disease

Foetal and neonatal energy metabolism in pigs and humans: a review

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