scholarly journals Is maternal obesity related to semen quality in the male offspring? A pilot study

2007 ◽  
Vol 22 (10) ◽  
pp. 2758-2762 ◽  
Author(s):  
C.H. Ramlau-Hansen ◽  
E.A. Nohr ◽  
A.M. Thulstrup ◽  
J.P. Bonde ◽  
L. Storgaard ◽  
...  
2002 ◽  
Vol 110 (3) ◽  
pp. 229-233 ◽  
Author(s):  
Russ Hauser ◽  
Larisa Altshul ◽  
Zuying Chen ◽  
Louise Ryan ◽  
James Overstreet ◽  
...  
Keyword(s):  

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
E. Chang ◽  
H. Hafner ◽  
M. Varghese ◽  
C. Griffin ◽  
J. Clemente ◽  
...  

Abstract With the increasing prevalence of obesity in women of reproductive age there is a need to understand the ramifications of this on offspring. The purpose of this study is to investigate the programming effects of maternal obesity during preconception and the preconception/gestational period on adiposity and adipose tissue inflammation in offspring using an animal model. Adult female C57Bl/6J mice were assigned either normal diet, high fat diet (HFD) prior to pregnancy, or HFD prior to and through pregnancy. Some offspring were maintained on normal diet while others started HFD later in life. Offspring were assessed for body composition and metabolic responses. Lipid storing tissues were evaluated for expansion and inflammation. Male offspring from the preconception group had the greatest weight gain, most subcutaneous adipose tissue, and largest liver mass when introduced to postnatal HFD. Male offspring of the preconception/gestation group had worsened glucose tolerance and an increase in resident (CD11c−) adipose tissue macrophages (ATMs) when exposed to postnatal HFD. Female offspring had no significant difference in any parameter between the diet treatment groups. In conclusion, this study demonstrates that prenatal and pregnancy windows have independent programming effects on offspring. Preconception exposure affects body composition and adiposity while gestation exposure affects metabolism and tissue immune cell phenotypes.


Andrologia ◽  
2020 ◽  
Vol 52 (4) ◽  
Author(s):  
Patrícia Pinto‐Pinho ◽  
Joana Matos ◽  
Regina Arantes‐Rodrigues ◽  
Zélia Gomes ◽  
Miguel Brito ◽  
...  

2019 ◽  
Vol 11 (1) ◽  
pp. 37-43 ◽  
Author(s):  
Sergio De los Santos ◽  
Luis Antonio Reyes-Castro ◽  
Ramón Mauricio Coral-Vázquez ◽  
Juan Pablo Méndez ◽  
Marcela Leal-García ◽  
...  

AbstractObjective:To determine whether (-)-epicatechin (Epi) could decrease visceral adipose tissue and improve the metabolic profile of male offspring rats, after maternal obesity was induced by a high-fat diet (HFD).Design:Maternal obesity in albino Wistar rats was induced with a HFD, whereas male offspring were fed with chow diet throughout the study. Eight male offspring per group, from different litters, were randomly assigned to the experimental or to the control groups. In the experimental group, Epi was administered at a dose of 1 mg/kg of body weight to the male offspring twice daily for two weeks, beginning at postnatal day (PND).Main measures:Weight of visceral adipose tissue, adipocyte size, and several metabolic parameters.Results:Epi administration in the male offspring induced a significant decrease in the amount of visceral fat (11.61 g less, P < 0.05) and in the size of adipose cells (28% smaller, P < 0.01). Besides, Epi was able to decrease insulin, leptin, and Homeostasis Model Assessment -Insulin Resistance (HOMA-IR) (P < 0.05), as well as triglycerides, when the experimental group was compared to the untreated male offspring of obese rats (P < 0.01).Conclusions:Epi administration can reverse the negative effects that maternal obesity has on the male offspring. This could be because Epi reduces the amount of visceral fat and improves metabolic profile.


2007 ◽  
Vol 166 (9) ◽  
pp. 1105-1105
Author(s):  
T. K. Jensen ◽  
N. Jorgensen ◽  
C. Asklund ◽  
N. E. Skakkebaek

2013 ◽  
Vol 60 (9) ◽  
pp. 507-512
Author(s):  
Maria G. Grammatikopoulou ◽  
Agathi A. Pritsa ◽  
Sophia Badeka ◽  
Irini Aggelaki ◽  
Ioanna Giantsiou ◽  
...  
Keyword(s):  

Chemosphere ◽  
2018 ◽  
Vol 198 ◽  
pp. 266-273 ◽  
Author(s):  
Yun-jiang Yu ◽  
Bi-gui Lin ◽  
Wei-bo Liang ◽  
Liang-zhong Li ◽  
Yu-de Hong ◽  
...  

2016 ◽  
Vol 230 (1) ◽  
pp. 39-53 ◽  
Author(s):  
Simon Lecoutre ◽  
Barbara Deracinois ◽  
Christine Laborie ◽  
Delphine Eberlé ◽  
Céline Guinez ◽  
...  

According to the Developmental Origin of Health and Disease (DOHaD) concept, alterations of nutrient supply in the fetus or neonate result in long-term programming of individual body weight (BW) setpoint. In particular, maternal obesity, excessive nutrition, and accelerated growth in neonates have been shown to sensitize offspring to obesity. The white adipose tissue may represent a prime target of metabolic programming induced by maternal obesity. In order to unravel the underlying mechanisms, we have developed a rat model of maternal obesity using a high-fat (HF) diet (containing 60% lipids) before and during gestation and lactation. At birth, newborns from obese dams (called HF) were normotrophs. However, HF neonates exhibited a rapid weight gain during lactation, a key period of adipose tissue development in rodents. In males, increased BW at weaning (+30%) persists until 3months of age. Nine-month-old HF male offspring was normoglycemic but showed mild glucose intolerance, hyperinsulinemia, and hypercorticosteronemia. Despite no difference in BW and energy intake, HF adult male offspring was predisposed to fat accumulation showing increased visceral (gonadal and perirenal) depots weights and hyperleptinemia. However, only perirenal adipose tissue depot exhibited marked adipocyte hypertrophy and hyperplasia with elevated lipogenic (i.e. sterol-regulated element binding protein 1 (Srebp1), fatty acid synthase (Fas), and leptin) and diminished adipogenic (i.e. peroxisome proliferator-activated receptor gamma (Pparγ), 11β-hydroxysteroid dehydrogenase type 1 (11β-Hds1)) mRNA levels. By contrast, very few metabolic variations were observed in HF female offspring. Thus, maternal obesity and accelerated growth during lactation program offspring for higher adiposity via transcriptional alterations of visceral adipose tissue in a depot- and sex-specific manner.


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