Literature DB >> 36164619

Increasing of LDH Specific Activity and PEPCK Level Play a Role on Activation of Gluconeogenesis Pathway in Early Onset Pre-Eeclampsia Placenta.

Syarifah Dewi1,2, Visabella Rizky Triatmono3, Puti Raykhan Rasyada Ralas3, Veraldi Veraldi3, Irvan M Alfian3, Febriana Catur Iswanti1,2, Ani Retno Prijanti1,2.   

Abstract

Background: Recent advancement on experiment concluded that etiology of pre-eclampsia (PE) could be explained by the "two-stage" theory. The theory of which explained that pre-eclampsia occurs due to abnormalities in spiral arteries development and release of inflammatory response. Failure of spiral arteries development, the lesion of damage could be due to ischemia-reperfusion or hypoxia-reoxygenation. Hypoxia in pre-eclamptic placenta leads to metabolic change to anaerobic in glycolysis. Lactate dehydrogenase (LDH) has important role in anaerobic glycolysis that catalyzes the conversion of lactate to pyruvate during hypoxia. On the other hand, phosphoenolpyruvate carboxy kinase (PEPCK) is merely an enzyme of gluconeogenesis. This research conduct to reveal that in early onset pre-eclampsia the placenta still hypoxic and undergoes gluconeogenesis even after delivery, through metabolic enzyme of LDH and PEPCK level.
Methods: This cross-sectional study compared early onset PE (< 34 weeks) with normal term placenta. We measured LDH enzyme activity using colorimetric assay and PEPCK protein using ELISA method.
Results: Result show that placental LDH specific activity was increased significantly in PE with median 2.750 (0.030 - 5.680) U/mg compared to normal term placenta 0.255 (0.032 - 1.194) U/mg (Mann-Whitney, p< 0.001). PEPCK level was significantly increased in PE 8.998 (1.737-44.914) ng/mg compared to normal term placenta 1.552 (0.741-8.832) ng/mg (Mann-Whitney, p< 0.001).
Conclusion: We conclude that anaerobic glycolysis and gluconeogenesis pathway are increased in early onset PE placenta as adaptation mechanism to hypoxic condition.

Entities:  

Keywords:  Early onset preeclampsia; LDH; PEPCK; Placenta

Year:  2022        PMID: 36164619      PMCID: PMC9455191          DOI: 10.52547/rbmb.11.2.320

Source DB:  PubMed          Journal:  Rep Biochem Mol Biol        ISSN: 2322-3480


  7 in total

1.  Failure of physiologic transformation of spiral arteries, endothelial and trophoblast cell activation, and acute atherosis in the basal plate of the placenta.

Authors:  Carlos A Labarrere; Hector L DiCarlo; Elaine Bammerlin; James W Hardin; Yeon M Kim; Piya Chaemsaithong; David M Haas; Ghassan S Kassab; Roberto Romero
Journal:  Am J Obstet Gynecol       Date:  2016-12-27       Impact factor: 8.661

Review 2.  Prevention and treatment of pregnancy-induced hypertension (preeclampsia) with progestogens.

Authors:  M B Sammour; H el-Kabarity; M M Fawzy; A E Schindler
Journal:  J Steroid Biochem Mol Biol       Date:  2005-10-19       Impact factor: 4.292

3.  Inhibition of HIF-1a-mediated TLR4 activation decreases apoptosis and promotes angiogenesis of placental microvascular endothelial cells during severe pre-eclampsia pathogenesis.

Authors:  Lina Zhao; Ruixia Ma; Li Zhang; Xiaolan Yuan; Jinhua Wu; Lirong He; Guocheng Liu; Rui Du
Journal:  Placenta       Date:  2019-06-15       Impact factor: 3.481

Review 4.  Pre-eclampsia: pathophysiology, diagnosis, and management.

Authors:  Jennifer Uzan; Marie Carbonnel; Olivier Piconne; Roland Asmar; Jean-Marc Ayoubi
Journal:  Vasc Health Risk Manag       Date:  2011-07-19

5.  Effects of stress during pregnancy on hepatic glucogenic capacity in rat dams and their fetuses.

Authors:  Kathryn L Franko; Alison J Forhead; Abigail L Fowden
Journal:  Physiol Rep       Date:  2017-06

Review 6.  Preeclampsia in 2018: Revisiting Concepts, Physiopathology, and Prediction.

Authors:  J Mayrink; M L Costa; J G Cecatti
Journal:  ScientificWorldJournal       Date:  2018-12-06

Review 7.  Pre-eclampsia: its pathogenesis and pathophysiolgy.

Authors:  P Gathiram; J Moodley
Journal:  Cardiovasc J Afr       Date:  2016 Mar-Apr       Impact factor: 1.167

  7 in total

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