MATERNAL OBESITY AND OXIDATIVE STRESS IN THE FETUS: MECHANISMS UNDERLYING EARLY LIFE SHIFTS IN SKELETAL MUSCLE METABOLISM

2011 ◽  
Vol 22 (3) ◽  
pp. 219-246
Author(s):  
KRISTEN E BOYLE ◽  
JACOB E FRIEDMAN
Keyword(s):  
Oxidative Stress ◽  
Risk Factor ◽  
Maternal Obesity ◽  
Muscle Metabolism ◽  
Obese Women ◽  
Maternal Risk ◽  
Metabolic Outcome ◽  
Underlying Risk Factor ◽  
Adipose Tissue Lipolysis ◽  
Underlying Risk

The most common maternal risk factor associated with neonatal complications during delivery is obesity. Although gestational diabetes mellitus (GDM) occurs in 5–10% of the pregnant population, obesity, by virtue of its prevalence, far outpaces GDM as the most important underlying risk factor for increased fetal adiposity. The mechanisms underlying maternal insulin resistance may play an important role in the diversion of excess fuels to the fetus. Maternal adipose depots increase in early pregnancy, followed by increased adipose tissue lipolysis and subsequent hyperlipidaemia, which mainly corresponds to increased triglyceride levels (TG). A positive correlation between maternal TG and infant body weight or fat mass has been found in both GDM and non-GDM obese women. Increased oxidative stress, altered adipokines, and inflammatory cytokines have also been found in obese pregnant women, suggesting an adverse metabolic outcome even in normoglycemic conditions.

Longitudinal associations between inhibitory control and externalizing and internalizing symptoms in school-aged children

2020 ◽  
pp. 1-13
Author(s):  
Katri Maasalo ◽  
Jallu Lindblom ◽  
Olli Kiviruusu ◽  
Päivi Santalahti ◽  
Eeva T. Aronen
Keyword(s):  
Risk Factor ◽  
Inhibitory Control ◽  
Internalizing Symptoms ◽  
Psychiatric Symptoms ◽  
Externalizing Symptoms ◽  
Causal Role ◽  
Trait Level ◽  
Underlying Risk Factor ◽  
Externalizing And Internalizing Symptoms ◽  
Underlying Risk

Abstract Inhibitory control (IC) deficits have been associated with psychiatric symptoms in all ages. However, longitudinal studies testing the direction of the associations in childhood are scarce. We used a sample of 2,874 children (7 to 9 years old) to test the following three hypotheses: (a) IC deficits are an underlying risk factor with a potentially causal role for psychopathology, (b) IC deficits are a complication of psychopathology, and (c) IC deficits and psychopathology are associated at the trait level but not necessarily causally related. We used the go/no-go task to assess IC, the parent-rated Strengths and Difficulties Questionnaire to evaluate externalizing/internalizing symptoms, and the random intercepts cross-lagged panel model to test the hypotheses. The results showed no support for the underlying risk factor hypothesis, suggesting that IC unlikely has a causal role in this age group's psychopathology. The complication hypothesis received support for externalizing symptoms, suggesting that externalizing symptoms may hamper the normal development of IC. IC deficits and both externalizing and internalizing symptoms were correlated at the trait level, indicating a possible common origin. We suggest that it may be useful to support children with externalizing symptoms to promote and protect their IC development.

scholarly journals Mitochondrial Ca2+ Overload Leads to Mitochondrial Oxidative Stress and Delayed Meiotic Resumption in Mouse Oocytes

2020 ◽  
Vol 8 ◽  
Author(s):  
Luyao Zhang ◽  
Zichuan Wang ◽  
Tengfei Lu ◽  
Lin Meng ◽  
Yan Luo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Function ◽  
Maternal Obesity ◽  
Polar Body ◽  
Germinal Vesicle ◽  
Oocyte Quality ◽  
Obese Women ◽  
Germinal Vesicle Breakdown ◽  
Mouse Oocytes ◽  
First Polar Body

Overweight or obese women seeking pregnancy is becoming increasingly common. Human maternal obesity gives rise to detrimental effects during reproduction. Emerging evidence has shown that these abnormities are likely attributed to oocyte quality. Oxidative stress induces poor oocyte conditions, but whether mitochondrial calcium homeostasis plays a key role in oocyte status remains unresolved. Here, we established a mitochondrial Ca2+ overload model in mouse oocytes. Knockdown gatekeepers of the mitochondrial Ca2+ uniporters Micu1 and Micu2 as well as the mitochondrial sodium calcium exchanger NCLX in oocytes both increased oocytes mitochondrial Ca2+ concentration. The overload of mitochondria Ca2+ in oocytes impaired mitochondrial function, leaded to oxidative stress, and changed protein kinase A (PKA) signaling associated gene expression as well as delayed meiotic resumption. Using this model, we aimed to determine the mechanism of delayed meiosis caused by mitochondrial Ca2+ overload, and whether oocyte-specific inhibition of mitochondrial Ca2+ influx could improve the reproductive abnormalities seen within obesity. Germinal vesicle breakdown stage (GVBD) and extrusion of first polar body (PB1) are two indicators of meiosis maturation. As expected, the percentage of oocytes that successfully progress to the germinal vesicle breakdown stage and extrude the first polar body during in vitro culture was increased significantly, and the expression of PKA signaling genes and mitochondrial function recovered after appropriate mitochondrial Ca2+ regulation. Additionally, some indicators of mitochondrial performance—such as adenosine triphosphate (ATP) and reactive oxygen species (ROS) levels and mitochondrial membrane potential—recovered to normal. These results suggest that the regulation of mitochondrial Ca2+ uptake in mouse oocytes has a significant role during oocyte maturation as well as PKA signaling and that proper mitochondrial Ca2+ reductions in obese oocytes can recover mitochondrial performance and improve obesity-associated oocyte quality.

Childhood venous thromboembolism—A careful look at complete blood count can reveal the underlying risk factor

2020 ◽  
Vol 67 (8) ◽  
Author(s):  
Aaqib Zaffar Banday ◽  
Reva Tyagi ◽  
Suchit Jogu ◽  
Murugan Sudhakar ◽  
Pratap Kumar Patra ◽  
...  
Keyword(s):  
Risk Factor ◽  
Venous Thromboembolism ◽  
Blood Count ◽  
Complete Blood Count ◽  
Underlying Risk Factor ◽  
Underlying Risk

scholarly journals Maternal Body Weight and Gestational Diabetes Differentially Influence Placental and Pregnancy Outcomes

2016 ◽  
Vol 101 (1) ◽  
pp. 59-68 ◽  
Author(s):  
J. Martino ◽  
S. Sebert ◽  
M. T. Segura ◽  
L. García-Valdés ◽  
J. Florido ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Birth Weight ◽  
Gestational Diabetes ◽  
Maternal Obesity ◽  
Antenatal Visit ◽  
Maternal Body Mass Index ◽  
Obese Women ◽  
Maternal Body ◽  
Energy Sensing

Abstract Context: Maternal obesity and gestational diabetes mellitus (GDM) can both contribute to adverse neonatal outcomes. The extent to which this may be mediated by differences in placental metabolism and nutrient transport remains to be determined. Objective: Our objective was to examine whether raised maternal body mass index (BMI) and/or GDM contributed to a resetting of the expression of genes within the placenta that are involved in energy sensing, oxidative stress, inflammation, and metabolic pathways. Methods: Pregnant women from Spain were recruited as part of the “Study of Maternal Nutrition and Genetics on the Foetal Adiposity Programming” survey at the first antenatal visit (12–20 weeks of gestation) and stratified according to prepregnancy BMI and the incidence of GDM. At delivery, placenta and cord blood were sampled and newborn anthropometry measured. Results: Obese women with GDM had higher estimated fetal weight at 34 gestational weeks and a greater risk of preterm deliveries and cesarean section. Birth weight was unaffected by BMI or GDM; however, women who were obese with normal glucose tolerance had increased placental weight and higher plasma glucose and leptin at term. Gene expression for markers of placental energy sensing and oxidative stress, were primarily affected by maternal obesity as mTOR was reduced, whereas SIRT-1 and UCP2 were both upregulated. In placenta from obese women with GDM, gene expression for AMPK was also reduced, whereas the downstream regulator of mTOR, p70S6KB1 was raised. Conclusions: Placental gene expression is sensitive to both maternal obesity and GDM which both impact on energy sensing and could modulate the effect of either raised maternal BMI or GDM on birth weight.

Normal-tension glaucoma and Alzheimer’s disease: Helicobacter pylori as a possible common underlying risk factor

2007 ◽  
Vol 68 (1) ◽  
pp. 228-229 ◽  
Author(s):  
Jannis Kountouras ◽  
Christos Zavos ◽  
Emmanuel Gavalas ◽  
Marina Boziki ◽  
Dimitrios Chatzopoulos ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Helicobacter Pylori ◽  
Risk Factor ◽  
Normal Tension Glaucoma ◽  
Underlying Risk Factor ◽  
Underlying Risk
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