Search Results

You are looking at 1 - 4 of 4 items for

  • Author: Adam J Watkins x
  • Refine by access: All content x
Clear All Modify Search
Aileen F Keating Department of Animal Science, Iowa State University, Ames, Iowa, USA

Search for other papers by Aileen F Keating in
Google Scholar
PubMed
Close
and
Adam J Watkins Division of Child Health, Obstetrics and Gynaecology, University of Nottingham School of Medicine, Nottingham, UK

Search for other papers by Adam J Watkins in
Google Scholar
PubMed
Close
Free access
Afsaneh Khoshkerdar Division of Child Health, Obstetrics and Gynaecology, Faculty of Medicine, University of Nottingham, Nottingham, UK

Search for other papers by Afsaneh Khoshkerdar in
Google Scholar
PubMed
Close
,
Ece Eryasar Division of Child Health, Obstetrics and Gynaecology, Faculty of Medicine, University of Nottingham, Nottingham, UK

Search for other papers by Ece Eryasar in
Google Scholar
PubMed
Close
,
Hannah L Morgan Division of Child Health, Obstetrics and Gynaecology, Faculty of Medicine, University of Nottingham, Nottingham, UK

Search for other papers by Hannah L Morgan in
Google Scholar
PubMed
Close
, and
Adam J Watkins Division of Child Health, Obstetrics and Gynaecology, Faculty of Medicine, University of Nottingham, Nottingham, UK

Search for other papers by Adam J Watkins in
Google Scholar
PubMed
Close

Pregnancy represents a time of dramatic physiological adaptation by the mother in which dramatic changes in maternal cardiovascular, metabolic and immune systems occur. These adaptations, initiated from the earliest stages of gestation, are crucial for the implantation and continued development of the embryo, the establishment of the placenta and the growth of the fetus. Impairments in the normal adaptation of the maternal cardiovascular, metabolic and immune systems underlie the aetiology of gestational disorders such as preeclampsia and gestational diabetes. Studies have shown that the development of such gestational complications not only affects the well-being of the mother but also the short- and long-term health of her offspring. While the connection between maternal lifestyle factors and the development of gestational disorders such as preeclampsia and gestational diabetes has been studied in detail, the link between a father’s lifestyle and the well-being of the mother during pregnancy has received less attention. In this review, we will explore the evidence that a range of paternal factors, such as age and diet, at the time of conception can not only affect the development of his offspring, but also the well-being of the mother during pregnancy. In addition, we will examine the sperm- and seminal plasma-specific mechanisms that connect the health of the father with that of the mother and his offspring.

Free access
Adam J Watkins Centre for Biological Sciences, School of Life and Health Sciences, Faculty of Life Sciences, Southampton General Hospital, University of Southampton, Southampton SO16 6YD, UK
Centre for Biological Sciences, School of Life and Health Sciences, Faculty of Life Sciences, Southampton General Hospital, University of Southampton, Southampton SO16 6YD, UK

Search for other papers by Adam J Watkins in
Google Scholar
PubMed
Close
,
Emma S Lucas Centre for Biological Sciences, School of Life and Health Sciences, Faculty of Life Sciences, Southampton General Hospital, University of Southampton, Southampton SO16 6YD, UK

Search for other papers by Emma S Lucas in
Google Scholar
PubMed
Close
,
Stephanie Marfy-Smith Centre for Biological Sciences, School of Life and Health Sciences, Faculty of Life Sciences, Southampton General Hospital, University of Southampton, Southampton SO16 6YD, UK

Search for other papers by Stephanie Marfy-Smith in
Google Scholar
PubMed
Close
,
Nicola Bates Centre for Biological Sciences, School of Life and Health Sciences, Faculty of Life Sciences, Southampton General Hospital, University of Southampton, Southampton SO16 6YD, UK

Search for other papers by Nicola Bates in
Google Scholar
PubMed
Close
,
Susan J Kimber Centre for Biological Sciences, School of Life and Health Sciences, Faculty of Life Sciences, Southampton General Hospital, University of Southampton, Southampton SO16 6YD, UK

Search for other papers by Susan J Kimber in
Google Scholar
PubMed
Close
, and
Tom P Fleming Centre for Biological Sciences, School of Life and Health Sciences, Faculty of Life Sciences, Southampton General Hospital, University of Southampton, Southampton SO16 6YD, UK

Search for other papers by Tom P Fleming in
Google Scholar
PubMed
Close

Mammalian placentation is dependent upon the action of trophoblast cells at the time of implantation. Appropriate fetal growth, regulated by maternal nutrition and nutrient transport across the placenta, is a critical factor for adult offspring long-term health. We have demonstrated that a mouse maternal low-protein diet (LPD) fed exclusively during preimplantation development (Emb-LPD) increases offspring growth but programmes adult cardiovascular and metabolic disease. In this study, we investigate the impact of maternal nutrition on post-implantation trophoblast phenotype and fetal growth. Ectoplacental cone explants were isolated at day 8 of gestation from female mice fed either normal protein diet (NPD: 18% casein), LPD (9% casein) or Emb-LPD and cultured in vitro. We observed enhanced spreading and cell division within proliferative and secondary trophoblast giant cells (TGCs) emerging from explants isolated from LPD-fed females when compared with NPD and Emb-LPD explants after 24 and 48 h. Moreover, both LPD and Emb-LPD explants showed substantial expansion of TGC area during 24–48 h, not observed in NPD. No difference in invasive capacity was observed between treatments using Matrigel transwell migration assays. At day 17 of gestation, LPD- and Emb-LPD-fed conceptuses displayed smaller placentas and larger fetuses respectively, resulting in increased fetal:placental ratios in both groups compared with NPD conceptuses. Analysis of placental and yolk sac nutrient signalling within the mammalian target of rapamycin complex 1 pathway revealed similar levels of total and phosphorylated downstream targets across groups. These data demonstrate that early post-implantation embryos modify trophoblast phenotype to regulate fetal growth under conditions of poor maternal nutrition.

Open access
Hannah L Morgan Division of Child Health, Obstetrics and Gynaecology, Faculty of Medicine, University of Nottingham, Nottingham, UK

Search for other papers by Hannah L Morgan in
Google Scholar
PubMed
Close
,
Isaac Ampong Faculty of Health and Medical Sciences, University of Surrey, Stag Hill, Guildford, UK

Search for other papers by Isaac Ampong in
Google Scholar
PubMed
Close
,
Nader Eid Division of Child Health, Obstetrics and Gynaecology, Faculty of Medicine, University of Nottingham, Nottingham, UK

Search for other papers by Nader Eid in
Google Scholar
PubMed
Close
,
Charlène Rouillon INRA, Fish Physiology and Genomics, Bat 16A, Campus de Beaulieu, Rennes, France

Search for other papers by Charlène Rouillon in
Google Scholar
PubMed
Close
,
Helen R Griffiths Faculty of Health and Medical Sciences, University of Surrey, Stag Hill, Guildford, UK

Search for other papers by Helen R Griffiths in
Google Scholar
PubMed
Close
, and
Adam J Watkins Division of Child Health, Obstetrics and Gynaecology, Faculty of Medicine, University of Nottingham, Nottingham, UK

Search for other papers by Adam J Watkins in
Google Scholar
PubMed
Close

The link between male diet and sperm quality has received significant investigation. However, the impact diet and dietary supplements have on the testicular environment has been examined to a lesser extent. Here, we establish the impact of a sub-optimal low protein diet (LPD) on testicular morphology, apoptosis and serum fatty acid profiles. Furthermore, we define whether supplementing a LPD with specific methyl donors abrogates any detrimental effects of the LPD. Male C57BL6 mice were fed either a control normal protein diet (NPD; 18% protein; n = 8), an isocaloric LPD (LPD; 9% protein; n = 8) or an LPD supplemented with methyl donors (MD-LPD; choline chloride, betaine, methionine, folic acid, vitamin B12; n = 8) for a minimum of 7 weeks. Analysis of male serum fatty acid profiles by gas chromatography revealed elevated levels of saturated fatty acids and lower levels of mono- and polyunsaturated fatty acids in MD-LPD males when compared to NPD and/or LPD males. Testes of LPD males displayed larger seminiferous tubule cross section area when compared to NPD and MD-LPD males, while MD-LPD tubules displayed a larger luminal area. Furthermore, TUNNEL staining revealed LPD males possessed a reduced number of tubules positive for apoptosis, while gene expression analysis showed MD-LPD testes displayed decreased expression of the pro-apoptotic genes Bax, Csap1 and Fas when compared to NPD males. Finally, testes from MD-LPD males displayed a reduced telomere length but increased telomerase activity. These data reveal the significance of sub-optimal nutrition for paternal metabolic and reproductive physiology.

Open access