Gluconeogenesis in the fetus and neonate

Kalhan, Satish C.; Parimi, Prabhu S.

doi:10.1053/sp.2000.6360

Cited by 151 publications

(99 citation statements)

References 60 publications

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“…This increase was shown to be due to an enhanced activity of PEPCK which results from decreased methylation of the gene's promoter [13]. Formerly, it was assumed that substantial gluconeogenesis only starts to occur` at birth [22], but more recent publications, using mammalian animal models of intrauterine growth restriction and inadequate maternal nutrition, point towards intra-uterine initiation of gluconeogenesis [13,23,24]. In fetal baboons it was shown that the PEPCK protein, a key enzyme in gluconeogenesis, was upregulated in MNR fetuses [13].…”

Section: 9gmentioning

confidence: 99%

Influence of moderate maternal nutrition restriction on the fetal baboon metabolome at 0.5 and 0.9 gestation

Hellmuth

Uhl

Kirchberg

et al. 2016

Nutrition, Metabolism and Cardiovascular Diseases

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Section: 9gmentioning

confidence: 99%

Influence of moderate maternal nutrition restriction on the fetal baboon metabolome at 0.5 and 0.9 gestation

Hellmuth

Uhl

Kirchberg

et al. 2016

Nutrition, Metabolism and Cardiovascular Diseases

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“…Chronic maternal HFD feeding reprograms the fetal hepatic gluconeogenic pathway. Hepatic gluconeogenesis is normally absent during fetal development, which is primarily attributed to the appearance of the rate-limiting enzyme phosphoenolpyruvate carboxykinase (PCK1) at the time of birth (58)(59)(60)(61)(62). Quantitative PCR demonstrated increased expression in 4 key enzymes in the gluconeogenic pathway in the O-HFD group: glucose 6 phosphatase (G6P), fructose 1,6-bisphosphatase 1 (FBP1), PPARγ coactivator 1α (PGC1A, which encodes PGC1α), and PCK1 (2-tailed Student's t test, Figure 4, A-D).…”

Section: Figurementioning

confidence: 99%

Maternal high-fat diet triggers lipotoxicity in the fetal livers of nonhuman primates

McCurdy¹,

Bishop²,

Williams³

et al. 2009

J. Clin. Invest.

420

562

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Maternal obesity is thought to increase the offspring's risk of juvenile obesity and metabolic diseases; however, the mechanism(s) whereby excess maternal nutrition affects fetal development remain poorly understood. Here, we investigated in nonhuman primates the effect of chronic high-fat diet (HFD) on the development of fetal metabolic systems. We found that fetal offspring from both lean and obese mothers chronically consuming a HFD had a 3-fold increase in liver triglycerides (TGs). In addition, fetal offspring from HFD-fed mothers (O-HFD) showed increased evidence of hepatic oxidative stress early in the third trimester, consistent with the development of nonalcoholic fatty liver disease (NAFLD). O-HFD animals also exhibited elevated hepatic expression of gluconeogenic enzymes and transcription factors. Furthermore, fetal glycerol levels were 2-fold higher in O-HFD animals than in control fetal offspring and correlated with maternal levels. The increased fetal hepatic TG levels persisted at P180, concurrent with a 2-fold increase in percent body fat. Importantly, reversing the maternal HFD to a low-fat diet during a subsequent pregnancy improved fetal hepatic TG levels and partially normalized gluconeogenic enzyme expression, without changing maternal body weight. These results suggest that a developing fetus is highly vulnerable to excess lipids, independent of maternal diabetes and/or obesity, and that exposure to this may increase the risk of pediatric NAFLD.

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“…Because plasma glucose homeostasis requires glucogenesis and ketogenesis to maintain normal rates of fuel use, 13 NH most commonly occurs in infants with impaired glucogenesis and/or ketogenesis, 14,15 which may occur with excessive insulin production, altered counterregulatory hormone production, an inadequate substrate supply, [14][15][16] or a disorder of fatty acid oxidation. 15 NH occurs most commonly in infants who are small for gestational age, infants born to mothers who have diabetes, and late-preterm infants.…”

Section: Which Infants To Screenmentioning

confidence: 99%

“…15 NH occurs most commonly in infants who are small for gestational age, infants born to mothers who have diabetes, and late-preterm infants. It remains controversial whether otherwise normal infants who are large for gestational age are at risk of NH, largely because it is difficult to exclude maternal diabetes or maternal hyperglycemia (prediabetes) with standard glucose-tolerance tests.…”

Section: Which Infants To Screenmentioning

confidence: 99%

Postnatal Glucose Homeostasis in Late-Preterm and Term Infants

Adamkin¹

2011

Pediatrics

603

278

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This report provides a practical guide and algorithm for the screening and subsequent management of neonatal hypoglycemia. Current evidence does not support a specific concentration of glucose that can discriminate normal from abnormal or can potentially result in acute or chronic irreversible neurologic damage. Early identification of the at-risk infant and institution of prophylactic measures to prevent neonatal hypoglycemia are recommended as a pragmatic approach despite the absence of a consistent definition of hypoglycemia in the literature.

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Gluconeogenesis in the fetus and neonate

Cited by 151 publications

References 60 publications

Influence of moderate maternal nutrition restriction on the fetal baboon metabolome at 0.5 and 0.9 gestation

Influence of moderate maternal nutrition restriction on the fetal baboon metabolome at 0.5 and 0.9 gestation

Maternal high-fat diet triggers lipotoxicity in the fetal livers of nonhuman primates

Postnatal Glucose Homeostasis in Late-Preterm and Term Infants

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