scholarly journals Prenatal exposure to maternal obesity leads to hyperactivity in offspring

2011 ◽  
Vol 17 (12) ◽  
pp. 1159-1160 ◽  
Author(s):  
C Fernandes ◽  
H Grayton ◽  
L Poston ◽  
A-M Samuelsson ◽  
P D Taylor ◽  
...  
Keyword(s):  
Prenatal Exposure ◽  
Maternal Obesity

scholarly journals Sex differences in the association between prenatal exposure to maternal obesity and hippocampal volume in children

2020 ◽  
Vol 10 (2) ◽  
Author(s):  
Jasmin M. Alves ◽  
Shan Luo ◽  
Ting Chow ◽  
Megan Herting ◽  
Anny H. Xiang ◽  
...  
Keyword(s):  
Sex Differences ◽  
Prenatal Exposure ◽  
Maternal Obesity ◽  
Hippocampal Volume

190-OR: Impact of Prenatal Exposure to Maternal Obesity and Child Physical Activity Levels on Neurocognition

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 190-OR
Author(s):  
JASMIN ALVES ◽  
BRENDAN C. ANGELO ◽  
SHAN H. LUO ◽  
TING CHOW ◽  
ALEXANDRA G. YUNKER ◽  
...  
Keyword(s):  
Physical Activity ◽  
Prenatal Exposure ◽  
Maternal Obesity ◽  
Activity Levels ◽  
Child Physical Activity ◽  
Physical Activity Levels

Prenatal Exposure to Maternal Obesity Alters Anxiety and Stress Coping Behaviors in Aged Mice

2015 ◽  
Vol 103 (3-4) ◽  
pp. 354-368 ◽  
Author(s):  
Georgia Balsevich ◽  
Valentin Baumann ◽  
Andres Uribe ◽  
Alon Chen ◽  
Mathias V. Schmidt
Keyword(s):  
Prenatal Exposure ◽  
Maternal Obesity ◽  
Stress Coping ◽  
Coping Behaviors ◽  
Aged Mice

Role of prenatal exposure to environmental pollutants and maternal obesity in fetal programming of chronic diseases in mice

Placenta ◽  
2015 ◽  
Vol 36 (4) ◽  
pp. 499-500
Author(s):  
F. Salas-Pérez ◽  
L. Berkowitz ◽  
K. Cautivo ◽  
A. Rigotti ◽  
M. Farías ◽  
...  
Keyword(s):  
Chronic Diseases ◽  
Prenatal Exposure ◽  
Fetal Programming ◽  
Maternal Obesity ◽  
Environmental Pollutants

Reversal of cardiomyopathy resulting from prenatal exposure to ethanol

1984 ◽  
Vol 42 ◽  
pp. 716-717
Author(s):  
C. Uphoff ◽  
C. Nyquist-Battie
Keyword(s):  
Prenatal Exposure ◽  
Heart Development ◽  
Membrane Integrity ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Pathological Changes ◽  
Prenatally Exposed ◽  
Inner Mitochondrial Membrane ◽  
Fetal Alcohol ◽  
Newborn Mice

Fetal Alcohol Syndrone (FAS) is a syndrome with characteristic abnormalities resulting from prenatal exposure to ethanol. In many children with FAS syndrome gross pathological changes in the heart are seen with septal defects the most prevalent abnormality recorded. Few studies in animal models have been performed on the effects of ethanol on heart development. In our laboratory, it has been observed that prenatal ethanol exposure of Swiss albino mice results in abnormal cardiac muscle ultrastructure when mice were examined at birth and compared to pairfed and normal controls. Fig. 1 is an example of the changes that are seen in the ethanol-exposed animals. These changes include enlarged mitochondria with loss of inner mitochondrial membrane integrity and loss of myofibrils. Morphometric analysis substantiated the presence of these alterations from normal cardiac ultrastructure. The present work was undertaken to determine if the pathological changes seen in the newborn mice prenatally exposed to ethanol could be reversed with age and abstinence.

The dual nature of obesity in metabolic programming: quantity versus quality of adipose tissue

2020 ◽  
Vol 134 (18) ◽  
pp. 2447-2451
Author(s):  
Anissa Viveiros ◽  
Gavin Y. Oudit
Keyword(s):  
Adipose Tissue ◽  
Environmental Factors ◽  
Maternal Obesity ◽  
Metabolic Programming ◽  
Dual Nature ◽  
Prevalence Of Obesity ◽  
Adipose Tissue Volume ◽  
Males And Females ◽  
Metabolically Healthy

Abstract The global prevalence of obesity has been rising at an alarming rate, accompanied by an increase in both childhood and maternal obesity. The concept of metabolic programming is highly topical, and in this context, describes a predisposition of offspring of obese mothers to the development of obesity independent of environmental factors. Research published in this issue of Clinical Science conducted by Litzenburger and colleagues (Clin. Sci. (Lond.) (2020) 134, 921–939) have identified sex-dependent differences in metabolic programming and identify putative signaling pathways involved in the differential phenotype of adipose tissue between males and females. Delineating the distinction between metabolically healthy and unhealthy obesity is a topic of emerging interest, and the precise nature of adipocytes are key to pathogenesis, independent of adipose tissue volume.

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