Reports of Biochemistry and Molecular Biology

en Increasing of LDH Specific Activity and PEPCK Level Play a Role on Activation of Gluconeogenesis Pathway in Early Onset Pre-Eeclampsia Placenta بیوشیمی Biochemistry مقالات اصلی Original Article <div style="text-align: justify;">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). Conclusions: We conclude that anaerobic glycolysis and gluconeogenesis pathway are increased in early onset PE placenta as adaptation mechanism to hypoxic condition.</div> Early onset preeclampsia, LDH, PEPCK, Placenta. 320 326 http://rbmb.net/browse.php?a_code=A-10-744-2&slc_lang=en&sid=1 Syarifah Dewi 100319475328460012843 100319475328460012843 No 1: Department of Biochemistry and Molecular Biology, Faculty of Medicine Universitas Indonesia, Jakarta, Indonesia & Center of Hypoxia and Oxidative Stress Studies, Faculty of Medicine Universitas Indonesia, Jakarta, Indonesia. Visabella Rizky Triatmono 100319475328460012844 100319475328460012844 No Undergraduate Program in Medical Sciences, Faculty Medicine Universitas Indonesia, Jl. Salemba Raya no. 6 Jakarta, 10430. Puti Raykhan Rasyada Ralas 100319475328460012845 100319475328460012845 No Undergraduate Program in Medical Sciences, Faculty Medicine Universitas Indonesia, Jl. Salemba Raya no. 6 Jakarta, 10430. Veraldi Veraldi 100319475328460012846 100319475328460012846 No Undergraduate Program in Medical Sciences, Faculty Medicine Universitas Indonesia, Jl. Salemba Raya no. 6 Jakarta, 10430. Irvan Alfian 100319475328460012847 100319475328460012847 No Undergraduate Program in Medical Sciences, Faculty Medicine Universitas Indonesia, Jl. Salemba Raya no. 6 Jakarta, 10430. Febriana Catur Iswanti 100319475328460012848 100319475328460012848 No 1: Department of Biochemistry and Molecular Biology, Faculty of Medicine Universitas Indonesia, Jakarta, Indonesia & Center of Hypoxia and Oxidative Stress Studies, Faculty of Medicine Universitas Indonesia, Jakarta, Indonesia. Ani Retno Prijanti aniretno@gmail.com 100319475328460012849 100319475328460012849 Yes 1: Department of Biochemistry and Molecular Biology, Faculty of Medicine Universitas Indonesia, Jakarta, Indonesia & Center of Hypoxia and Oxidative Stress Studies, Faculty of Medicine Universitas Indonesia, Jakarta, Indonesia.