scholarly journals Maternal Obesity Increases Oxidative Stress in Placenta and It Is Associated With Intestinal Microbiota

2021 ◽  
Vol 11 ◽  
Author(s):  
Chengjun Hu ◽  
Yingli Yan ◽  
Fengjie Ji ◽  
Hanlin Zhou
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Intestinal Microbiota ◽  
Maternal Obesity ◽  
Citrate Synthase ◽  
Obese Group ◽  
Backfat Thickness ◽  
Microbiota Composition ◽  
Placental Dysfunction ◽  
Placental Oxidative Stress

Maternal obesity induces placental dysfunction and intestinal microbial dysbiosis. However, the associations between intestinal microbiota and placental dysfunction are still unclear. In the present study, a gilt model was used to investigate the role of maternal obesity on placental oxidative stress, mitochondrial function, and fecal microbiota composition, meanwhile identifying microbiota markers associated with placental oxidative stress. Twenty gilts were divided into two groups based on their backfat thickness on parturition day: namely Con group (average backfat thickness = 33 mm), and Obese group (average backfat thickness = 39 mm). The results showed that Obese group was lower than Con group in the birth weight of piglets. Compared with the Con group, the Obesity group exhibited an increased oxidative damage and inflammatory response in placenta, as evidenced by the increased concentrations of placental reactive oxygen species (ROS), protein carboxyl, and interleukin-6 (IL-6). Obesity group was lower than Con group in the concentrations of placental adenosine triphosphate, citrate synthase, and complex I activity. In addition, lower propionate level and Bacteroidetes abundance in feces were seen in the Obese Group. Furthermore, the concentrations of placental ROS, protein carboxyl, and IL-6 were positively correlated with the abundance of Christensenellaceae_R-7_group and negatively correlated with that of norank_f_Bacteroidales_S24-7_group. In conclusion, these findings suggest that maternal obesity might impair oxidative and inflammatory response in placenta through modulating intestinal microbiota composition.

scholarly journals Angiogenesis in the Placenta: The Role of Reactive Oxygen Species Signaling

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Robyn D. Pereira ◽  
Nicole E. De Long ◽  
Ruijun C. Wang ◽  
Fereshteh T. Yazdi ◽  
Alison C. Holloway ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factors ◽  
Maternal Obesity ◽  
Placental Development ◽  
Placental Dysfunction ◽  
Placental Angiogenesis ◽  
Healthy Pregnancy ◽  
Adverse Pregnancy ◽  
And Function ◽  
Reactive Oxygen Species Signaling

Proper placental development and function are central to the health of both the mother and the fetus during pregnancy. A critical component of healthy placental function is the proper development of its vascular network. Poor vascularization of the placenta can lead to fetal growth restriction, preeclampsia, and in some cases fetal death. Therefore, understanding the mechanisms by which uterine stressors influence the development of the placental vasculature and contribute to placental dysfunction is of central importance to ensuring a healthy pregnancy. In this review we discuss how oxidative stress observed in maternal smoking, maternal obesity, and preeclampsia has been associated with aberrant angiogenesis and placental dysfunction resulting in adverse pregnancy outcomes. We also highlight that oxidative stress can influence the expression of a number of transcription factors important in mediating angiogenesis. Therefore, understanding how oxidative stress affects redox-sensitive transcription factors within the placenta may elucidate potential therapeutic targets for correcting abnormal placental angiogenesis and function.

scholarly journals Palmitic acid induces inflammation in placental trophoblasts and impairs their migration toward smooth muscle cells through plasminogen activator inhibitor-1

2020 ◽  
Vol 26 (11) ◽  
pp. 850-865
Author(s):  
Amanda M Rampersaud ◽  
Caroline E Dunk ◽  
Stephen J Lye ◽  
Stephen J Renaud
Keyword(s):  
Smooth Muscle ◽  
Inflammatory Response ◽  
Smooth Muscle Cells ◽  
Palmitic Acid ◽  
Maternal Obesity ◽  
Muscle Cells ◽  
Trophoblast Invasion ◽  
Migration And Invasion ◽  
Placental Development ◽  
Placental Dysfunction

Abstract A critical component of early human placental development includes migration of extravillous trophoblasts (EVTs) into the decidua. EVTs migrate toward and displace vascular smooth muscle cells (SMCs) surrounding several uterine structures, including spiral arteries. Shallow trophoblast invasion features in several pregnancy complications including preeclampsia. Maternal obesity is a risk factor for placental dysfunction, suggesting that factors within an obese environment may impair early placental development. Herein, we tested the hypothesis that palmitic acid, a saturated fatty acid circulating at high levels in obese women, induces an inflammatory response in EVTs that hinders their capacity to migrate toward SMCs. We found that SMCs and SMC-conditioned media stimulated migration and invasion of an EVT-like cell line, HTR8/SVneo. Palmitic acid impaired EVT migration and invasion toward SMCs, and induced expression of several vasoactive and inflammatory mediators in EVTs, including endothelin, interleukin (IL)-6, IL-8 and PAI1. PAI1 was increased in plasma of women with early-onset preeclampsia, and PAI1-deficient EVTs were protected from the anti-migratory effects of palmitic acid. Using first trimester placental explants, palmitic acid exposure decreased EVT invasion through Matrigel. Our findings reveal that palmitic acid induces an inflammatory response in EVTs and attenuates their migration through a mechanism involving PAI1. High levels of palmitic acid in pathophysiological situations like obesity may impair early placental development and predispose to placental dysfunction.

Dietary methionine restriction improves the gut microbiota and reduces intestinal permeability and inflammation in high-fat-fed mice

2019 ◽  
Vol 10 (9) ◽  
pp. 5952-5968 ◽  
Author(s):  
Yuhui Yang ◽  
Yuanhong Zhang ◽  
Yuncong Xu ◽  
Tingyu Luo ◽  
Yueting Ge ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gut Microbiota ◽  
Intestinal Permeability ◽  
Intestinal Microbiota ◽  
Barrier Function ◽  
Microbiota Composition ◽  
High Fat ◽  
Methionine Restriction

Dietary methionine restriction improved the intestinal microbiota composition, barrier function, oxidative stress, and inflammation in high-fat-fed mice.

scholarly journals Palmitic acid induces inflammation in placental trophoblasts and impairs their migration toward smooth muscle cells through plasminogen activator inhibitor-1

2020 ◽  
Author(s):  
Amanda M. Rampersaud ◽  
Caroline E. Dunk ◽  
Stephen J. Lye ◽  
Stephen J. Renaud
Keyword(s):  
Smooth Muscle ◽  
Inflammatory Response ◽  
Smooth Muscle Cells ◽  
Palmitic Acid ◽  
Maternal Obesity ◽  
Muscle Cells ◽  
Trophoblast Invasion ◽  
Migration And Invasion ◽  
Placental Development ◽  
Placental Dysfunction

AbstractA critical component of early human placental development includes migration of extravillous trophoblasts (EVTs) into the decidua. EVTs migrate toward, and displace vascular smooth muscle cells (SMCs) surrounding several uterine structures, including spiral arteries. Shallow trophoblast invasion features in several pregnancy complications including preeclampsia. Maternal obesity is a risk factor for placental dysfunction, suggesting that factors within an obese environment may impair early placental development. Herein, we tested the hypothesis that palmitic acid, a saturated fatty acid circulating at high levels in obese women, induces an inflammatory response in EVTs that hinders their capacity to migrate toward SMCs. We found that SMCs and SMC-conditioned media stimulated migration and invasion of an EVT-like cell line, HTR8/SVneo. Palmitic acid impaired EVT migration and invasion toward SMCs, and induced expression of several vasoactive and inflammatory mediators in EVTs, including endothelin, interleukin (IL)-6, IL8, and PAI1. PAI1 was increased in plasma of women with early-onset preeclampsia, and PAI1-deficient EVTs were protected from the anti-migratory effects of palmitic acid. Using first trimester placental explants, palmitic acid exposure decreased EVT invasion through Matrigel. Our findings reveal that palmitic acid induces an inflammatory response in EVTs and attenuates their migration through a mechanism involving PAI1. High levels of palmitic acid in pathophysiological situations like obesity may impair early placental development and predispose to placental dysfunction.

scholarly journals Gut-Muscle Axis Exists and May Affect Skeletal Muscle Adaptation to Training

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1451 ◽  
Author(s):  
Katarzyna Przewłócka ◽  
Marcin Folwarski ◽  
Karolina Kaźmierczak-Siedlecka ◽  
Karolina Skonieczna-Żydecka ◽  
Jan Jacek Kaczor
Keyword(s):  
Oxidative Stress ◽  
Immune System ◽  
Intestinal Microbiota ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Glycogen Storage ◽  
Microbiota Composition ◽  
Muscle Adaptation ◽  
Chronic Oxidative Stress ◽  
And Function

Excessive training may limit physiological muscle adaptation through chronic oxidative stress and inflammation. Improper diet and overtraining may also disrupt intestinal homeostasis and in consequence enhance inflammation. Altogether, these factors may lead to an imbalance in the gut ecosystem, causing dysregulation of the immune system. Therefore, it seems to be important to optimize the intestinal microbiota composition, which is able to modulate the immune system and reduce oxidative stress. Moreover, the optimal intestinal microbiota composition may have an impact on muscle protein synthesis and mitochondrial biogenesis and function, as well as muscle glycogen storage. Aproperly balanced microbiome may also reduce inflammatory markers and reactive oxygen species production, which may further attenuate macromolecules damage. Consequently, supplementation with probiotics may have some beneficial effect on aerobic and anaerobic performance. The phenomenon of gut-muscle axis should be continuously explored to function maintenance, not only in athletes.

Naringin Inhibits TNF-α Induced Oxidative Stress and Inflammatory Response in HUVECs via Nox4/NF-κ B and PI3K/Akt Pathways

2014 ◽  
Vol 15 (12) ◽  
pp. 1173-1182 ◽  
Author(s):  
Wenshuang Li ◽  
Changyuan Wang ◽  
Jinyong Peng ◽  
Jing Liang ◽  
Yue Jin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response

scholarly journals 145 President Oral Presentation Pick: Prenatal stress increases skeletal muscle mitochondrial volume density and function in yearling Brahman calves

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 120-121
Author(s):  
Chloey P Guy ◽  
Catherine L Wellman ◽  
David G Riley ◽  
Charles R Long ◽  
Ron D Randel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Creatine Kinase ◽  
Muscle Damage ◽  
Prenatal Stress ◽  
Citrate Synthase ◽  
Volume Density ◽  
Assembly Factor ◽  
Mitochondrial Volume ◽  
Mitochondrial Volume Density ◽  
And Function

Abstract We previously determined that prenatal stress (PNS) differentially affected methylation of DNA from leukocytes of 28-d-old calves. Specifically, COX14 (cytochrome c oxidase (COX) assembly factor) and CKMT1B (mitochondrial creatine kinase U-type) were hypomethylated and COA5 (COX assembly factor 5), COX5A (COX subunit 5A), NRF1 (nuclear respiratory factor 1), and GSST1 (glutathione S-transferase theta-1) were hypermethylated in PNS compared to non-PNS calves (P ≤ 0.05). Our current objective was to test the hypothesis that PNS exhibit impaired mitochondrial function and greater oxidative stress than non-PNS calves. Blood and longissimus dorsi muscle samples were collected from yearling Brahman calves whose mothers were stressed by 2 h transportation at 60, 80, 100, 120, and 140 days of gestation (PNS; 8 bulls, 6 heifers) and non-PNS calves (4 bulls, 6 heifers). Serum was evaluated for the stress hormone, cortisol, and muscle damage marker, creatine kinase; muscle was analyzed for mitochondrial volume density and function by citrate synthase (CS) and COX activities, respectively, concentration of malondialdehyde, a lipid peroxidation marker, and activity of the antioxidant, superoxide dismutase (SOD). Data were analyzed using mixed linear models with treatment and sex as fixed effects. Serum cortisol was numerically higher in PNS than non-PNS calves but was not statistically different. Muscle CS and COX activities relative to protein were greater in PNS than non-PNS calves (P ≤ 0.03), but COX relative to CS activity was similar between groups. Activity of COX was greater in bulls than heifers (P = 0.03), but no other measure was affected by sex. All other measures were unaffected by PNS. Prenatal stress did not affect markers of muscle damage and oxidative stress in yearling Brahman calves at rest but mitochondrial volume density and function were greater in PNS calves. Acute stressors induce oxidative stress, so implications of differences in mitochondria in PNS calves following a stressor should be investigated.

scholarly journals High-fat diet-induced obesity and impairment of brain neurotransmitter pool

2020 ◽  
Vol 11 (1) ◽  
pp. 147-160
Author(s):  
Ranyah Shaker M. Labban ◽  
Hanan Alfawaz ◽  
Ahmed T. Almnaizel ◽  
Wail M. Hassan ◽  
Ramesa Shafi Bhat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Tissue ◽  
High Fat Diet ◽  
Density Lipoprotein ◽  
Obese Group ◽  
Control Group ◽  
High Fat ◽  
Brain Neurotransmitter ◽  
The Brain ◽  
Lean Group

AbstractObesity and the brain are linked since the brain can control the weight of the body through its neurotransmitters. The aim of the present study was to investigate the effect of high-fat diet (HFD)-induced obesity on brain functioning through the measurement of brain glutamate, dopamine, and serotonin metabolic pools. In the present study, two groups of rats served as subjects. Group 1 was fed a normal diet and named as the lean group. Group 2 was fed an HFD for 4 weeks and named as the obese group. Markers of oxidative stress (malondialdehyde, glutathione, glutathione-s-transferase, and vitamin C), inflammatory cytokines (interleukin [IL]-6 and IL-12), and leptin along with a lipid profile (cholesterol, triglycerides, high-density lipoprotein, and low-density lipoprotein levels) were measured in the serum. Neurotransmitters dopamine, serotonin, and glutamate were measured in brain tissue. Fecal samples were collected for observing changes in gut flora. In brain tissue, significantly high levels of dopamine and glutamate as well as significantly low levels of serotonin were found in the obese group compared to those in the lean group (P > 0.001) and were discussed in relation to the biochemical profile in the serum. It was also noted that the HFD affected bacterial gut composition in comparison to the control group with gram-positive cocci dominance in the control group compared to obese. The results of the present study confirm that obesity is linked to inflammation, oxidative stress, dyslipidemic processes, and altered brain neurotransmitter levels that can cause obesity-related neuropsychiatric complications.

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