Changes in activity of enzymes related to glycolysis, gluconeogenesis and lipogenesis in placentae from diabetic women

Diamant, Yoram Z.; Kissilevitz, Rita; Shafrir, Eleazar

doi:10.1016/s0143-4004(84)80048-x

Cited by 13 publications

(7 citation statements)

References 17 publications

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“…High Pyruvate Kinase activity has been found both in rat and human placentae, indicating that the placenta is having a high glycolytic potential [37]–[38]. This was indeed the case, since further results on placentae in women with gestational diabetes showed increased Pyruvate Kinase activity [39]–[40]. A large meta-analysis involving pregnant women with PCOS demonstrated an increase in the prevalence of gestational diabetes compared to pregnant women without PCOS [6].…”

Section: Discussionmentioning

confidence: 97%

Proteomic Biomarkers of Preterm Birth Risk in Women with Polycystic Ovary Syndrome (PCOS): A Systematic Review and Biomarker Database Integration

et al. 2013

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BackgroundPreterm Birth (PTB) is a major cause of neonatal mortality and morbidity. Women with Polycystic Ovary Syndrome (PCOS) are at high risk of PTB. There is a need for research studies to investigate the mechanisms linking PCOS and PTB, to facilitate screening, and develop novel preventative strategies.ObjectiveTo list all the proteomic biomarkers of PTB and integrate this list with the PCOS biomarker database to identify commonly expressed biomarkers of the two conditions.Search StrategyA systematic review of PTB biomarkers and update of PCOS biomarker database. All eligible published studies on proteomic biomarkers for PTB and PCOS identified through various databases were evaluated.Selection CriteriaFor the identification of the relevant studies, the following search terms were used: “proteomics”, “proteomic”, “preterm birth”, “preterm labour”, “proteomic biomarker” and “polycystic ovary syndrome”. This search was restricted to humans onlyData Collection and AnalysisA database on proteomic biomarkers for PTB was created while an already existing PCOS biomarker database was updated. The two databases were integrated and biomarkers that were co-expressed in both women with PCOS and PTB were identified and investigated.ResultsA panel of six proteomic biomarkers was similarly differentially expressed in women with PTB and women with PCOS compared to their respective controls (normal age-matched women in the case of PCOS studies and women with term pregnancy in the case of PTB studies). These biomarkers include Pyruvate kinase M1/M2, Vimentin, Fructose bisphosphonate aldolase A, Heat shock protein beta-1, Peroxiredoxin-1 and Transferrin.ConclusionsThese proteomic biomarkers (Pyruvate kinase M1/M2, Vimentin, Fructose bisphosphonate aldolase A, Heat shock protein beta-1, Peroxiredoxin-1 and Transferrin) can be potentially used to better understand the pathophysiological mechanisms linking PCOS and PTB. This would help to identify subgroups of women with PCOS at risk of PTB and hence the potential of developing preventative strategies.

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Section: Discussionmentioning

confidence: 97%

Proteomic Biomarkers of Preterm Birth Risk in Women with Polycystic Ovary Syndrome (PCOS): A Systematic Review and Biomarker Database Integration

et al. 2013

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“…The placenta also accumulates lipids, both in the diabetic rat [61 ] and human [14], although no change was found in the levels of placental enzymes regulating lipogenesis [13,15,48]. Once in the fetal circulation, these excess lipids contribute to fetal adipos ity [61], However, fetal hyperinsulism is known to stimulate fatty acid synthesis in many tissues [34,41,44,75] and to cause obesity even in fetuses of normal rats [2].…”

Section: Studies In Diabetesmentioning

confidence: 99%

Placental Transfer of Non-Esterified Fatty Acids in Normal and Diabetic Pregnancy

Thomas¹

1987

Neonatology

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The placental transfer of non-esterified fatty acids, predominantly in the direction of mother to fetus, is regulated on a gross scale by the transplacental non-esterified fatty acid gradient. This is maintained by fetal liver lipid uptake and by enhanced lipolysis of circulating triacylglycerol in the pregnant mother. It is also dependent upon maternal placental blood flow, which is reduced in diabetes, upon the fetal umbilical blood flow, upon maternal and fetal albumin concentrations and upon intratrophoblastic fatty acid binding protein, which appears to be altered in diabetes. Circulating maternal tnacylglycerols also directly contribute non-esterified fatty acids to the fetus by intraplacental hydrolysis and the hypertriglyceridaemia associated with maternal diabetes, in concert with changes in lipase levels will enhance maternal to fetal lipid flux.

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“…This transfer could be altered, however, by changes in GLUT activity and/or syncytiotrophoblast consumption of glucose by glycolysis and/or glycogen synthesis. Indeed, changes in glycolytic, gluconeogenic and NADP-generating enzymes have been reported in diabetes [13]. Therefore it is important when assessing placental handling of glucose to consider not only transport, but also placental utilisation of glucose.…”

mentioning

confidence: 99%

Effects of gestational diabetes on human placental glucose uptake, transfer, and utilisation

et al. 2000

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Both pregestational [1] and gestational diabetes mellitus [2,3] can lead to neonatal macrosomia which is associated with fetal death, prematurity, birth trauma, and neonatal respiratory distress syndrome, hypoglycaemia, polycythaemia, hyperbilirubinaemia, hypocalcaemia, hypomagnesaemia and cardiomyopathy [4±6]. For macrosomic neonates, birth weight has not been consistently shown to positively correlate with the degree of control of maternal blood glucose [7,8], suggesting that factors other than or in addition to maternal blood glucose are associated with adverse clinical outcomes during diabetes in pregnancy.Offspring from pregnant women with diabetes are more likely to develop diabetes mellitus and obesity later in life. This observation and evidence that development of diabetes is more closely related to maternal than paternal health, suggests that the intrauterine environment is possibly of importance [9, 10]. Abstract Aims/hypothesis. Gestational diabetes is associated with complications for the offspring before, during and after delivery. Poor maternal glucose control, however, is a weak predictor of these complications. Given its position at the interface of the maternal and fetal circulations, the placenta possibly plays a crucial part in protecting the fetus from adverse effects from the maternal diabetic milieu. We hypothesised that gestational diabetes may result in changes in placental function, particularly with respect to the uptake, transfer, and/or utilisation of glucose. We aimed to examine glucose transport and utilisation in intact human placental lobules from women with gestational diabetes and those from normal pregnancies. Method. Dual perfusion of an isolated placental lobule was done on placentae from diet treated gestational diabetic (n = 7) and normal pregnant patients (n = 9) using maternal glucose concentrations of 4, 8,

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Changes in activity of enzymes related to glycolysis, gluconeogenesis and lipogenesis in placentae from diabetic women

Cited by 13 publications

References 17 publications

Proteomic Biomarkers of Preterm Birth Risk in Women with Polycystic Ovary Syndrome (PCOS): A Systematic Review and Biomarker Database Integration

Proteomic Biomarkers of Preterm Birth Risk in Women with Polycystic Ovary Syndrome (PCOS): A Systematic Review and Biomarker Database Integration

Placental Transfer of Non-Esterified Fatty Acids in Normal and Diabetic Pregnancy

Effects of gestational diabetes on human placental glucose uptake, transfer, and utilisation

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