Effect of dexamethasone on fetal hepatic glutamine-glutamate exchange

Timmerman, Michelle; Teng, Cecilia; Wilkening, Randall B.; Fennessey, Paul V.; Battaglia, Frederick C.; Meschia, Giacomo

doi:10.1152/ajpendo.2000.278.5.e839

Cited by 22 publications

(31 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The control data for hepatic and umbilical uptakes are in good agreement with previous measurements (3,5,8,12,13,18,23,25). However, this is the first study in which the fetal hepatic uptakes of glucose and all major glucogenic substrates have been measured in the same experimental preparation.…”

Section: Discussionsupporting

confidence: 88%

“…We conclude that fetal hepatic pyruvate and glutamate output is part of an adaptation to placental function that requires the fetal liver to maintain both a high rate of catabolism of glucogenic substrates and a low rate of gluconeogenesis. fetal liver; placenta; glutamate; fetal gluconeogenesis UNDER NORMAL PHYSIOLOGICAL CONDITIONS, the liver of the ovine fetus releases glutamate in the fetal circulation (18,23,25). About one-third of the glutamate released is produced from hydrolysis of plasma glutamine (25), and the remainder is produced via hepatic oxidative metabolism.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Fetal hepatic and umbilical uptakes of glucogenic substrates during a glucagon-somatostatin infusion

Teng

Battaglia

Meschia

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

Self Cite

View full text Add to dashboard Cite

Wilkening. Fetal hepatic and umbilical uptakes of glucogenic substrates during a glucagon-somatostatin infusion. Am J Physiol Endocrinol Metab 282: E542-E550, 2002; 10.1152/ajpendo.00248.2001.-To test the hypothesis that fetal hepatic glutamate output diverts the products of hepatic amino acid metabolism from hepatic gluconeogenesis, ovine fetal hepatic and umbilical uptakes of glucose and glucogenic substrates were measured before and during fetal glucagonsomatostatin (GS) infusion and during the combined infusion of GS, alanine, glutamine, and arginine. Before the infusions, hepatic uptake of lactate, alanine, glutamine, arginine, and other substrates was accompanied by hepatic output of pyruvate, aspartate, serine, glutamate, and ornithine. The GS infusion induced hepatic output of 1.00 Ϯ 0.07 mol glucose carbon/mol O 2 uptake, an equivalent reduction in hepatic output of pyruvate and glutamate carbon, a decrease in umbilical glucose uptake and placental uptake of fetal glutamate, an increase in hepatic alanine and arginine clearances, and a decrease in umbilical alanine, glutamine, and arginine uptakes. The latter result suggests that glucagon inhibits umbilical amino acid uptake. We conclude that fetal hepatic pyruvate and glutamate output is part of an adaptation to placental function that requires the fetal liver to maintain both a high rate of catabolism of glucogenic substrates and a low rate of gluconeogenesis. fetal liver; placenta; glutamate; fetal gluconeogenesis UNDER NORMAL PHYSIOLOGICAL CONDITIONS, the liver of the ovine fetus releases glutamate in the fetal circulation (18,23,25). About one-third of the glutamate released is produced from hydrolysis of plasma glutamine (25), and the remainder is produced via hepatic oxidative metabolism. The fetal infusion of uniformly labeled [ 13 C]lactate results in the appearance of hepatic venous glutamate, which is labeled mostly with either one or two 13

show abstract

Section: Discussionsupporting

confidence: 88%

mentioning

confidence: 99%

Fetal hepatic and umbilical uptakes of glucogenic substrates during a glucagon-somatostatin infusion

Teng

Battaglia

Meschia

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

Self Cite

View full text Add to dashboard Cite

show abstract

“…Increased steroid exposure in utero has been demonstrated to affect fetal and placental metabolism, nutrient transfer and endocrine function (Milley 1996, Timmerman et al 2000, Challis et al 2002. Fetal glucocorticoid exposure is a strong candidate for involvement in programming of the metabolic syndrome and has been shown to affect development in a range of organisms (Seckl 2008).…”

Section: Exposure To Sex Steroidsmentioning

confidence: 99%

Sex differences in developmental programming models

2013

View full text Add to dashboard Cite

The theory of developmental programming suggests that diseases such as the metabolic syndrome may be 'programmed' by exposure to adverse stimuli during early development. The developmental programming literature encompasses the study of a wide range of suboptimal intrauterine environments in a variety of species and correlates these with diverse phenotypic outcomes in the offspring. At a molecular level, a large number of variables have been measured and suggested as the basis of the programmed phenotype. The range of both dependent and independent variables studied often makes the developmental programming literature complex to interpret and the drawing of definitive conclusions difficult. A common, though under-explored, theme of many developmental programming models is a sex difference in offspring outcomes. This holds true across a range of interventions, including dietary, hypoxic, and surgical models. The molecular and phenotypic outcomes of adverse in utero conditions are often more prominent in male than female offspring, although there is little consideration given to the basis for this observation in most studies. We review the evidence that maternal energy investment in male and female conceptuses may not be equal and may be environment dependent. It is suggested that male and female development could be viewed as separate processes from the time of conception, with differences in both timing and outcomes.Reproduction (2013) 145 R1-R13

show abstract

“…In addition, in response to glucocorticoid treatment of either the mother or fetus, there are changes in the placental handling of certain amino acids such as alanine, glutamine and glutamate. However, there have been few studies on the effects of glucocorticoids on amino acid transporters in the placenta of any species to date [61,62]. Additionally, glucocorticoids change the production and metabolism of hormones by the placenta such as prostaglandins, placental lactogen, leptin, corticotrophin-releasing hormone (CRH), estrogens, progesterone and other progestagens [63,64].…”

Section: Introductionmentioning

confidence: 99%