scholarly journals Lipotoxicity in obese pregnancy and its potential role in adverse pregnancy outcome and obesity in the offspring

2010 ◽  
Vol 119 (3) ◽  
pp. 123-129 ◽  
Author(s):  
Eleanor Jarvie ◽  
Sylvie Hauguel-de-Mouzon ◽  
Scott M. Nelson ◽  
Naveed Sattar ◽  
Patrick M. Catalano ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Fatty Acids ◽  
Endothelial Dysfunction ◽  
Maternal Obesity ◽  
Adverse Pregnancy Outcome ◽  
Oxidized Lipids ◽  
Lower Body ◽  
Adverse Pregnancy ◽  
And Oxidative Stress

Increasing maternal obesity is a challenge that has an impact on all aspects of female reproduction. Lean and obese pregnant women gain similar fat mass, but lean women store fat in the lower-body compartment and obese women in central compartments. In the non-pregnant, central storage of fat is associated with adipocyte hypertrophy and represents a failure to adequately store excess fatty acids, resulting in metabolic dysregulation and ectopic fat accumulation (lipotoxicity). Obese pregnancy is associated with exaggerated metabolic adaptation, endothelial dysfunction and increased risk of adverse pregnancy outcome. We hypothesize that the preferential storage of fat in central rather than ‘safer’ lower-body depots in obese pregnancy leads to lipotoxicity. The combination of excess fatty acids and oxidative stress leads to the production of oxidized lipids, which can be cytotoxic and influence gene expression by acting as ligands for nuclear receptors. Lipid excess and oxidative stress provoke endothelial dysfunction. Oxidized lipids can inhibit trophoblast invasion and influence placental development, lipid metabolism and transport and can also affect fetal developmental pathways. As lipotoxicity has the capability of influencing both maternal endothelial function and placental function, it may link maternal obesity and placentally related adverse pregnancy outcomes such as miscarriage and pre-eclampsia. The combination of excess/altered lipid nutrient supply, suboptimal in utero metabolic environment and alterations in placental gene expression, inflammation and metabolism may also induce obesity in the offspring.

scholarly journals A Prospective Cohort Study providing Insights for Markers of Adverse Pregnancy Outcome in Women of Advanced Maternal Age

2020 ◽  
Author(s):  
Samantha Lean ◽  
Rebecca Jones ◽  
Stephen Roberts ◽  
Alexander Heazell
Keyword(s):  
Oxidative Stress ◽  
Pregnancy Outcome ◽  
Maternal Age ◽  
Adverse Outcome ◽  
Adverse Pregnancy Outcome ◽  
Advanced Maternal Age ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Adverse Pregnancy ◽  
And Oxidative Stress

Abstract Background Advanced maternal age (AMA; ≥35 years) is associated with increased rates of adverse pregnancy outcome. Better understanding of underlying pathophysiological processes may improve identification of AMA mothers who are at greatest risk of adverse outcome. This study aimed to investigate changes in oxidative stress and inflammation in AMA women and identify clinical and biochemical predictors of adverse pregnancy outcome in women of AMA.Methods The Manchester Advanced Maternal Age Study (MAMAS) was a multicentre, observational, prospective cohort study of 527 mothers. Participants were divided into three age groups for comparison 20-30 years (n=158), 35-39 years (n=212) and ≥40 years (n=157). Demographic and medical data were collected along with maternal blood samples at 28 and 36 weeks’ gestation. Multivariable analysis was conducted to identify variables associated with adverse outcome, defined as one or more of: small for gestational age (<10th centile), FGR (<5th centile), stillbirth, NICU admission, preterm birth <37 weeks gestation or Apgar score <7 at 5 minutes. Biomarkers of inflammation, oxidative stress and placental dysfunction were quantified in maternal serum. Univariate and multivariable statistical analyses were used to identify associations with composite adverse fetal outcome.Results: Maternal smoking was associated with adverse outcome in older mothers (Adjusted Odds Ratio (AOR) 4.34, 95% Confidence Interval (95%CI) 1.88, 9.99), whereas multiparity reduced the odds (AOR 0.56, 95% CI 0.34, 0.99). In uncomplicated AMA pregnancies, lower circulating anti-inflammatory IL-10, IL-RA and increased antioxidant capacity (TAC) were seen. In AMA with adverse outcome, TAC and oxidative stress markers were increased and levels of maternal circulating placental hormones (hPL, PlGF and sFlt-1) were reduced (p<0.05). Of these, placental growth factor had the strongest predictive accuracy (Area Under the Receiver Operator Characteristic (AUROC) = 0.74) followed by TAC (AUROC=0.69).Conclusions: This study identified alterations in circulating inflammatory and oxidative stress markers in AMA women and in AMA women with adverse pregnancy outcome providing preliminary evidence of mechanistic links. Further, larger studies are required to determine if these markers can be developed into a predictive model of an individual AMA woman’s risk of APO, enabling a reduction in stillbirth rates whilst minimising unnecessary intervention.

scholarly journals A prospective cohort study providing insights for markers of adverse pregnancy outcome in older mothers

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Samantha C. Lean ◽  
Rebecca L. Jones ◽  
Stephen A. Roberts ◽  
Alexander E. P. Heazell
Keyword(s):  
Oxidative Stress ◽  
Older Women ◽  
Pregnancy Outcome ◽  
Maternal Age ◽  
Adverse Outcome ◽  
Adverse Pregnancy Outcome ◽  
Older Mothers ◽  
Stress Markers ◽  
Adverse Pregnancy ◽  
And Oxidative Stress

Abstract Background Advanced maternal age (≥35 years) is associated with increased rates of adverse pregnancy outcome. Better understanding of underlying pathophysiological processes may improve identification of older mothers who are at greatest risk. This study aimed to investigate changes in oxidative stress and inflammation in older women and identify clinical and biochemical predictors of adverse pregnancy outcome in older women. Methods The Manchester Advanced Maternal Age Study (MAMAS) was a multicentre, observational, prospective cohort study of 528 mothers. Participants were divided into three age groups for comparison 20–30 years (n = 154), 35–39 years (n = 222) and ≥ 40 years (n = 152). Demographic and medical data were collected along with maternal blood samples at 28 and 36 weeks’ gestation. Multivariable analysis was conducted to identify variables associated with adverse outcome, defined as one or more of: small for gestational age (< 10th centile), FGR (<5th centile), stillbirth, NICU admission, preterm birth < 37 weeks’ gestation or Apgar score < 7 at 5 min. Biomarkers of inflammation, oxidative stress and placental dysfunction were quantified in maternal serum. Univariate and multivariable logistic regression was used to identify associations with adverse fetal outcome. Results Maternal smoking was associated with adverse outcome irrespective of maternal age (Adjusted Odds Ratio (AOR) 4.22, 95% Confidence Interval (95%CI) 1.83, 9.75), whereas multiparity reduced the odds (AOR 0.54, 95% CI 0.33, 0.89). In uncomplicated pregnancies in older women, lower circulating anti-inflammatory IL-10, IL-RA and increased antioxidant capacity (TAC) were seen. In older mothers with adverse outcome, TAC and oxidative stress markers were increased and levels of maternal circulating placental hormones (hPL, PlGF and sFlt-1) were reduced (p < 0.05). However, these biomarkers only had modest predictive accuracy, with the largest area under the receiver operator characteristic (AUROC) of 0.74 for placental growth factor followed by TAC (AUROC = 0.69). Conclusions This study identified alterations in circulating inflammatory and oxidative stress markers in older women with adverse outcome providing preliminary evidence of mechanistic links. Further, larger studies are required to determine if these markers can be developed into a predictive model of an individual older woman’s risk of adverse pregnancy outcome, enabling a reduction in stillbirth rates whilst minimising unnecessary intervention.

Treatment with n-3 polyunsaturated fatty acids reverses endothelial dysfunction and oxidative stress in experimental menopause

2013 ◽  
Vol 24 (1) ◽  
pp. 371-379 ◽  
Author(s):  
Gianluca Gortan Cappellari ◽  
Pasquale Losurdo ◽  
Sara Mazzucco ◽  
Emiliano Panizon ◽  
Mitja Jevnicar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Endothelial Dysfunction ◽  
Polyunsaturated Fatty Acids ◽  
And Oxidative Stress

Prevention of Endothelial Dysfunction and Cardiovascular Disease by n-3 Fatty Acids-Inhibiting Action on Oxidative Stress and Inflammation

2020 ◽  
Vol 26 (30) ◽  
pp. 3652-3666 ◽  
Author(s):  
Kazuo Yamagata
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Endothelial Cell ◽  
Endothelial Dysfunction ◽  
Vascular Endothelial Cells ◽  
Cell Damage ◽  
Epidemiological Studies ◽  
Vascular Endothelial ◽  
Epa And Dha ◽  
And Oxidative Stress

Background: Prospective cohort studies and randomized controlled trials have shown the protective effect of n-3 fatty acids against cardiovascular disease (CVD). The effect of n-3 fatty acids on vascular endothelial cells indicates their possible role in CVD prevention. Objective: Here, we describe the effect of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) on endothelial dysfunction-caused by inflammation and oxidative stress-and their role in the development of CVD. Methods: We reviewed epidemiological studies done on n-3 fatty acids in CVD. The effect of DHA and EPA on vascular endothelial cells was examined with regard to changes in various markers, such as arteriosclerosis, inflammation, and oxidative stress, using cell and animal models. Results: Epidemiological studies revealed that dietary intake of EPA and DHA was associated with a reduced risk of various CVDs. EPA and DHA inhibited various events involved in arteriosclerosis development by preventing oxidative stress and inflammation associated with endothelial cell damage. In particular, EPA and DHA prevented endothelial cell dysfunction mediated by inflammatory responses and oxidative stress induced by events related to CVD. DHA and EPA also increased eNOS activity and induced nitric oxide production. Conclusion: The effects of DHA and EPA on vascular endothelial cell damage and dysfunction may involve the induction of nitric oxide, in addition to antioxidant and anti-inflammatory effects. n-3 fatty acids inhibit endothelial dysfunction and prevent arteriosclerosis. Therefore, the intake of n-3 fatty acids may prevent CVDs, like myocardial infarction and stroke.

Omega-3 fatty acids and mood stabilizers alter behavioral and oxidative stress parameters in animals subjected to fenproporex administration

2016 ◽  
Vol 32 (2) ◽  
pp. 519-528 ◽  
Author(s):  
Lara M. Gomes ◽  
Milena Carvalho-Silva ◽  
Letícia J. Teixeira ◽  
Joyce Rebelo ◽  
Isabella T. Mota ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Mood Stabilizers ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Oxidative Stress Parameters ◽  
And Oxidative Stress ◽  
Stress Parameters

scholarly journals GTP Cyclohydrolase I Gene Polymorphisms Are Associated with Endothelial Dysfunction and Oxidative Stress in Patients with Type 2 Diabetes Mellitus

PLoS ONE ◽  
2014 ◽  
Vol 9 (11) ◽  
pp. e108587 ◽  
Author(s):  
Pawel P. Wolkow ◽  
Wladyslaw Kosiniak-Kamysz ◽  
Grzegorz Osmenda ◽  
Grzegorz Wilk ◽  
Beata Bujak-Gizycka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Endothelial Dysfunction ◽  
Gene Polymorphisms ◽  
Gtp Cyclohydrolase I ◽  
And Oxidative Stress ◽  
I Gene

scholarly journals Targeting ROS/NF-κB sigaling pathway by the seedless black Vitis vinifera polyphenols in CCl4-intoxicated kidney, lung, brain, and spleen in rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Noha H. Habashy ◽  
Ahmad S. Kodous ◽  
Marwa M. Abu-Serie
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Vitis Vinifera ◽  
Rat Kidney ◽  
Environmental Pollutant ◽  
Enhancing Effect ◽  
Tnf Α ◽  
Cox 2 ◽  
Histopathological Studies ◽  
And Oxidative Stress

AbstractCarbon tetrachloride (CCl4) is an abundant environmental pollutant that can generate free radicals and induce oxidative stress in different human and animal organs like the kidney, lung, brain, and spleen, causing toxicity. The present study evaluated the alleviative mechanism of the isolated polyphenolic fraction from seedless (pulp and skin) black Vitis vinifera (VVPF) on systemic oxidative and necroinflammatory stress in CCl4-intoxicated rats. Here, we found that the administration of VVPF to CCl4-intoxicated rats for ten days was obviously ameliorated the CCl4-induced systemic elevation in ROS, NO and TBARS levels, as well as MPO activity. Also, it upregulated the cellular activities of the enzymatic (SOD, and GPx) and non-enzymatic (TAC and GSH) antioxidants. Furthermore, the gene expression of the ROS-related necroinflammatory mediators (NF-κB, iNOS, COX-2, and TNF-α) in the kidney, brain, and spleen, as well as IL-1β, and IL-8 in the lung were greatly restored. The histopathological studies confirmed these biochemical results and showed a noticeable enhancing effect in the architecture of the studied organs after VVPF intake. Thus, this study indicated that VVPF had an alleviative effect on CCl4-induced necroinflammation and oxidative stress in rat kidney, lung, brain, and spleen via controlling the ROS/NF-κB pathway.

Mercury Exposure and Endothelial Dysfunction

2015 ◽  
Vol 34 (4) ◽  
pp. 300-307 ◽  
Author(s):  
Swati Omanwar ◽  
M. Fahim
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Vascular Endothelium ◽  
Circulatory System ◽  
Vital Role ◽  
Mercury Exposure ◽  
And Function ◽  
The Impact ◽  
And Oxidative Stress

Vascular endothelium plays a vital role in the organization and function of the blood vessel and maintains homeostasis of the circulatory system and normal arterial function. Functional disruption of the endothelium is recognized as the beginning event that triggers the development of consequent cardiovascular disease (CVD) including atherosclerosis and coronary heart disease. There is a growing data associating mercury exposure with endothelial dysfunction and higher risk of CVD. This review explores and evaluates the impact of mercury exposure on CVD and endothelial function, highlighting the interplay of nitric oxide and oxidative stress.

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