Fasting serum triglycerides, free fatty acids, and malondialdehyde are increased in preeclampsia, are positively correlated, and decrease within 48 hours post partum

Hubel, Carl A.; McLaughlin, Margaret K.; Evans, Rhobert W.; Hauth, Beth Ann; Sims, Cynthia J.; Roberts, James M.

doi:10.1016/s0002-9378(96)70336-8

Cited by 292 publications

(162 citation statements)

References 23 publications

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“…23,26 High amounts of H 2 O 2 generated as a consequence of increased levels of superoxide anion, can promote an increment in catalase activity that would eliminate the peroxides. The previously described increment in lipolysis activity in preeclampsia 27 is evident in our study with the significant increase noted in FFA levels in HDP as compared with PCW; promoted oxidative stress would allow LDL oxidation. A non-significant elevation of ox-LDL was found in HDP compared with PCW.…”

Section: Discussionsupporting

confidence: 79%

Abnormal levels of antioxidant defenses in a large sample of patients with hypertensive disorders of pregnancy

et al. 2011

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Increased levels of oxidative stress have been demonstrated in Preeclampsia in previous studies, but this finding has not been established in other hypertensive disorders in pregnancy (HDP). We measured different markers of lipid peroxidation and antioxidant defenses by spectrophotometry or enzymoimmunoanalysis in 339 pregnant women: 85 with gestational hypertension (GH), 88 chronic hypertension (CH), 104 Preeclampsia and 62 healthy pregnant control women (PCW). Lower activity of superoxide dismutase and higher levels of catalase were found in GH, CH and preeclampsia compared with PCW (964.4±116.5, 970.0±120.4, 971.2±137.5 and 1063.4±133.7 U g À1 Hb, Po0.001; and 313.0±71.7, 292.2±45.3, 297.1 ± 47.2, 215.5 ± 26.2 U mg À1 Hb, Po0.0001; respectively). Regarding the glutathione REDOX cycle, we found the following in GH, CH and preeclampsia compared with PCW: a decrease in its reduced form (2.6 ± 0.6, 2.7 ± 0.8, 2.7 ± 0.9, 3.3±1.3 lmol l À1 , Po0.003), a parallel increase in the oxidized form (185.6±68.9, 194.7±75.0, 184.3±78.3, 85.1±27.5 lmol l À1 , Po0.0001) and an increment in glutathione peroxidase (85.9±22.0, 86.4±20.9, 82.1±23.5 and 77.2 ± 19.7 U g À1 Hb, Po0.04) and glutathione reductase (6384.3 ± 1261.9, 6724.6 ± 1154.1, 6287.9 ± 1399.9 and 6044.4±1208.4 mU g À1 Hb, Po0.01, respectively). Nitrites/nitrates were higher in patients with preeclampsia than in PCW (31.50±15.08, 26.80±8.39 lmol l À1 , Po0.002). Although malondialdehyde and oxidized-LDL levels were similar among groups, free fatty acids were increased in every HDP (GH 514.6 ± 194.6, CH 501.3 ± 197.4, preeclampsia 555.2 ± 230.1 lmol l À1 ) compared with PCW (351.4 ± 146.1 lmol l À1 ), Po0.0001. Our results show an oxidation/reduction imbalance with an increase in oxidative stress coupled with a decreased capacity of antioxidant systems, not only in preeclampsia but also in every HDP.

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Section: Discussionsupporting

confidence: 79%

Abnormal levels of antioxidant defenses in a large sample of patients with hypertensive disorders of pregnancy

et al. 2011

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“…Increased triglyceride levels are a well-known independent risk factor for CVD, 20 and increased triglyceride levels has also been reported in PE. [21][22][23] We propose that increased triglyceride levels caused by the downregulation of ACOX2 to be a possible shared genetic risk factor for PE and CVD. Peroxisomes are one of the main locations for lipid metabolism in human beings.…”

Section: Discussionmentioning

confidence: 99%

Identification of ACOX2 as a shared genetic risk factor for preeclampsia and cardiovascular disease

et al. 2011

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Preeclampsia (PE) is a serious complication of pregnancy, which is highly correlated with later life cardiovascular disease (CVD). Many risk factors are common for both diseases, but the contribution of shared genes remains to be determined. In this study, we used an integrative strategy to assess lipid traits as risk factors for PE and CVD by whole genome transcriptional profiling performed on Norwegian decidua basalis tissues (N¼95) from preeclamptic and normal pregnancies and on blood lymphocytes (N¼1240) from the San Antonio Family Heart Study (SAFHS). Among 222 genes that were differentially expressed (false discovery rate (FDR) P-value o0.05) between the PE, cases and controls, we found one gene, ACOX2 (acyl-coenzyme A oxidase 2, branched chain), that was downregulated in PE whose transcription was also inversely correlated with triglyceride levels (P¼5.6Â10 À7 ; FDR P-value¼0.0002) in SAFHS. We further report associations between SNPs in the ACOX2 gene and the transcription level (P-value¼0.0045) of the gene, as well as with triglyceride levels (P-value¼0.0051). ACOX2 is involved in bile acid production, a process that has been associated with both oxidative stress and regulation of triglyceride levels. Oxidative stress and increased triglyceride levels are known risk factors for CVD and both have also been associated with PE. Our results suggest that downregulation of ACOX2 is a shared risk factor for PE and CVD.

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“…66 Many of the risk factors that predispose to the functional endothelial alterations of atherosclerosis also come into play in PE. Elevated homocysteine, 67 elevated triglycerides 68 with associated small dense low-density lipoprotein (LDL), 69 and insulin resistance 70 are all associated with increased risk for both disorders. Some of these changes such as elevated homocysteine persist beyond pregnancy, yet the PE syndrome and the attendant endothelial dysfunction abate with delivery.…”

Section: Effects On Ex Vivo Vesselsmentioning

confidence: 99%

Hypertension in pregnancy

Pipkin

Roberts

2000

J Hum Hypertens

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Hypertension arising during pregnancy remains one of the two most frequently-cited causes of maternal death in the UK. In some cases, pregnancy is unmasking underlying hypertension, which manifests itself in later life. Pregnant women who develop de novo proteinuric hypertension (pre-eclampsia, PE) can share many risk factors with patients with the metabolic syndrome, such as obesity, dyslipidaemia and insulin resistance. However, more than half the women who develop PE remain normotensive thereafter. There is a genetic component(s) to the disease, but it is most improbable that there is a 'PE gene'. Rather, there are factors such as geneticallydetermined thrombophilias which are predisposers but not prerequisites. Impaired placentation is a feature, with inadequate invasion of the spiral arteries by syncytiotrophoblast and poor remodelling. However, similiar features are found in association with non-hypertensive

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Fasting serum triglycerides, free fatty acids, and malondialdehyde are increased in preeclampsia, are positively correlated, and decrease within 48 hours post partum

Cited by 292 publications

References 23 publications

Abnormal levels of antioxidant defenses in a large sample of patients with hypertensive disorders of pregnancy

Abnormal levels of antioxidant defenses in a large sample of patients with hypertensive disorders of pregnancy

Identification of ACOX2 as a shared genetic risk factor for preeclampsia and cardiovascular disease

Hypertension in pregnancy

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