Prenatal Exposure to Dexamethasone in the Mouse Alters Cardiac Growth Patterns and Increases Pulse Pressure in Aged Male Offspring

Phthalates are ubiquitous environmental chemicals with endocrine disrupting properties and potentially obesogenic effects. We hypothesised that antenatal phthalate exposure may influence growth and adiposity patterns in girls through childhood into adolescence. Among 1342 Raine Study singleton females, 462 had maternal serum and at least one outcome available up to 20 years of age. Individuals’ maternal serum collected at 18 and 34 weeks gestation was pooled and analyzed for concentrations of 32 metabolites of 15 phthalate diesters. Cox regression and linear models were used to determine associations between maternal phthalate levels and age at menarche, change in height and weight z-scores between birth and two years, height from birth to 20 years, BMI from two to 20 years, deviation from mid-parental height at age 20 and DEXA scan measures at age 20. Weak negative associations were detected with some phthalate metabolites and change in height and weight z-score during infancy. Weak positive associations between some of the high molecular weight phthalate metabolites and height z-score were detected during childhood. While still within the normal range, age at menarche was slightly delayed in girls with higher prenatal exposure to the higher molecular weight phthalate metabolites. We derived some associations between prenatal phthalate exposure with early growth patterns and age at menarche.

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Prenatal Exposure to Gutkha, a Globally Relevant Smokeless Tobacco Product, Induces Hepatic Changes in Adult Mice

International Journal of Environmental Research and Public Health ◽

10.3390/ijerph17217895 ◽

2020 ◽

Vol 17 (21) ◽

pp. 7895

Author(s):

Shannon Doherty Lyons ◽

Jason L. Blum ◽

Carol Hoffman-Budde ◽

Pamela B. Tijerina ◽

M. Isabel Fiel ◽

...

Keyword(s):

Liver Disease ◽

Fatty Liver ◽

Hepatic Fibrosis ◽

Prenatal Exposure ◽

Adult Male ◽

Smokeless Tobacco ◽

Fatty Liver Disease ◽

Male Offspring ◽

Adult Offspring ◽

Dependent Manner

Maternal exposures during pregnancy affect the onset and progression of adult diseases in the offspring. A prior mouse study indicated that maternal tobacco smoke exposure affects hepatic fibrosis in adult offspring. Gutkha, a broadly used smokeless tobacco (ST) product, is widely used by pregnant woman in many countries. The objective of this murine study was to evaluate whether oral maternal exposure to gutkha during pregnancy alters non-alcoholic fatty liver disease (NAFLD) in adult offspring: risk factors for the progression of NAFLD to cirrhosis in adults remain elusive. Buccal cavity ‘painting’ of pregnant mice with gutkha began on gestational days (GD) 2–4 and continued until parturition. Beginning at 12 weeks of age, a subset of offspring were transitioned to a high-fat diet (HFD). Results demonstrated that prenatal exposure to gutkha followed by an HFD in adulthood significantly increased the histologic evidence of fatty liver disease only in adult male offspring. Changes in hepatic fibrosis-related cytokines (interleukin (IL)-1b and IL-6) and in hepatic collagen mRNA expression were observed when comparing adult male offspring exposed to gutkha in utero to those not exposed. These findings indicate that maternal use of gutkha during pregnancy affects NAFLD in adult offspring in a sex-dependent manner.

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The effects of prenatal exposure to a ‘junk food’ diet on offspring food preferences and fat deposition can be mitigated by improved nutrition during lactation

Journal of Developmental Origins of Health and Disease ◽

10.1017/s2040174413000330 ◽

2013 ◽

Vol 4 (5) ◽

pp. 348-357 ◽

Cited By ~ 21

Author(s):

J. R. Gugusheff ◽

M. Vithayathil ◽

Z. Y. Ong ◽

B. S. Muhlhausler

Keyword(s):

Prenatal Exposure ◽

Fat Mass ◽

Food Preferences ◽

Female Offspring ◽

Male Offspring ◽

Free Access ◽

Junk Food ◽

Suckling Period ◽

Diet Induced Obesity ◽

Cross Fostering

Exposure to a maternal junk food (JF) diet in utero and during the suckling period has been demonstrated to increase the preference for palatable food and increase the susceptibility to diet-induced obesity in adult offspring. We aimed to determine whether the effects of prenatal exposure to JF could be ameliorated by cross-fostering offspring onto dams consuming a standard rodent chow during the suckling period. We report here that when all offspring were given free access to the JF diet for 7 weeks from 10 weeks of age, male offspring of control (C) or JF dams that were cross-fostered at birth onto JF dams (C-JF, JF-JF), exhibited higher fat (C-C: 12.3 ± 0.34 g/kg/day; C-JF: 14.7 ± 1.04 g/kg/day; JF-C: 11.5 ± 0.41 g/kg/day; JF-JF: 14.0 ± 0.44 g/kg/day; P < 0.05) and overall energy intake (C-C: 930.1 ± 18.56 kJ/kg/day; C-JF: 1029.0 ± 82.9 kJ/kg/day; JF-C: 878.3 ± 19.5 kJ/kg/day; JF-JF: 1003.4 ± 25.97 kJ/kg/day; P < 0.05) than offspring exposed to the JF diet only before birth (JF-C) or not at all (C-C). Female offspring suckled by JF dams, despite no differences in food intake, had increased fat mass as percentage of body weight (C-C: 19.9 ± 1.33%; C-JF: 22.8 ± 1.57%; JF-C: 17.4 ± 1.03%; JF-JF: 22.0 ± 1.0%; P < 0.05) after 3 weeks on the JF diet. No difference in fat mass was observed in male offspring. These findings suggest that the effects of prenatal exposure to a JF diet on food preferences in females and susceptibility to diet-induced obesity in males can be prevented by improved nutrition during the suckling period.

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Prenatal exposure to lps leads to long-lasting physiological consequences in male offspring

Developmental Psychobiology ◽

10.1002/dev.20568 ◽

2011 ◽

Vol 53 (8) ◽

pp. 828-838 ◽

Cited By ~ 19

Author(s):

Masoud Asiaei ◽

Jalal Solati ◽

Ali-Akbar Salari

Keyword(s):

Prenatal Exposure ◽

Male Offspring

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Prenatal exposure to ambient fine particulate matter induces dysregulations of lipid metabolism in adipose tissue in male offspring

The Science of The Total Environment ◽

10.1016/j.scitotenv.2018.12.007 ◽

2019 ◽

Vol 657 ◽

pp. 1389-1397 ◽

Cited By ~ 9

Author(s):

Peisi Xie ◽

Chao Zhao ◽

Wei Huang ◽

Ting Yong ◽

Arthur C.K. Chung ◽

...

Keyword(s):

Adipose Tissue ◽

Particulate Matter ◽

Lipid Metabolism ◽

Prenatal Exposure ◽

Fine Particulate Matter ◽

Male Offspring ◽

Fine Particulate

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Prenatal Exposure to Blue and Green Colors Increases Serum Testosterone Levels in Male Offspring Rats

Biomedical & Pharmacology Journal ◽

10.13005/bpj/462 ◽

2014 ◽

Vol 7 (1) ◽

pp. 129-135

Author(s):

Padera Faryadyan ◽

Afra Khosravi ◽

Meysam Kashiri ◽

Reza Valizadeh

Keyword(s):

Prenatal Exposure ◽

Serum Testosterone ◽

Male Offspring ◽

Testosterone Levels

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Population Dynamics of Male-Killing and Non-Male-Killing Spiroplasmas in Drosophila melanogaster

Applied and Environmental Microbiology ◽

10.1128/aem.69.3.1428-1434.2003 ◽

2003 ◽

Vol 69 (3) ◽

pp. 1428-1434 ◽

Cited By ~ 73

Author(s):

Hisashi Anbutsu ◽

Takema Fukatsu

Keyword(s):

Population Dynamics ◽

Drosophila Melanogaster ◽

Adult Emergence ◽

Growth Patterns ◽

Male Offspring ◽

Adult Females ◽

Male Killing ◽

Short Period ◽

Selective Death ◽

Peak Value

ABSTRACT The endosymbiotic bacteria Spiroplasma spp. are vertically transmitted through female hosts and are known to cause selective death of male offspring in insects. One strain of spiroplasma, NSRO, causes male killing in Drosophila species, and a non-male-killing variant of NSRO, designated NSRO-A, has been isolated. It is not known why NSRO-A does not kill males. In an attempt to understand the mechanism of male killing, we investigated the population dynamics of NSRO and NSRO-A throughout the developmental course of the laboratory host Drosophila melanogaster by using a quantitative PCR technique. In the early development of the host insect, the titers of NSRO were significantly higher than those of NSRO-A at the first- and second-instar stages, whereas at the egg, third-instar, and pupal stages, the titers of the two spiroplasmas were almost the same. Upon adult emergence, the titers of the two spiroplasmas were similar, around 2 × 108 dnaA copy equivalents. However, throughout host aging, the two spiroplasmas showed strikingly different population growth patterns. The titers of NSRO increased exponentially for 3 weeks, attained a peak value of around 4 × 109 dnaA copy equivalents per insect, and then decreased. In contrast, the titers of NSRO-A were almost constant throughout the adult portion of the life cycle. In adult females, consequently, the titer of NSRO was significantly higher than the titer of NSRO-A except for a short period just after emergence. Although infection of adult females with NSRO resulted in almost 100% male killing, production of some male offspring was observed within 4 days after emergence when the titers of NSRO were as low as those of NSRO-A. Based on these results, we proposed a threshold density hypothesis for the expression of male killing caused by the spiroplasma. The extents of the bottleneck in the vertical transmission through host generations were estimated to be 5 × 10−5 for NSRO and 3 × 10−4 for NSRO-A.

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