Intergenerational transmission of programmed effects: public health consequences

Drake, Amanda J.; Liu, Lincoln

doi:10.1016/j.tem.2009.11.006

Cited by 95 publications

(86 citation statements)

References 86 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…We believe that the patterns of maternal investment in Babesia-treated females in our study could reflect immunocompetence-directed investment. Females may be specifically priming offspring for life in an environment in which the risk of infection is high [9]. Our results add to a growing body of evidence that suggests that effects of this sort occur across a wide range of taxa.…”

Section: Discussionmentioning

confidence: 54%

“…'Foetal programming' as a result of maternal exposure to disease or malnutrition, for example, has been shown to have diverse consequences for the health of children and even grandchildren [9]. Such maternal effects in humans are typically thought of as being detrimental to offspring fitness, but in studies of other species there has been more focus on potentially adaptive priming of offspring [2,10].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Infection before pregnancy affects immunity and response to social challenge in the next generation

Curno

Reader

McElligott

et al. 2011

Phil. Trans. R. Soc. B

View full text Add to dashboard Cite

Natural selection should favour parents that are able to adjust their offspring's life-history strategy and resource allocation in response to changing environmental and social conditions. Pathogens impose particularly strong and variable selective pressure on host life histories, and parental genes will benefit if offspring are appropriately primed to meet the immunological challenges ahead. Here, we investigated transgenerational immune priming by examining reproductive resource allocation by female mice in response to direct infection with Babesia microti prior to pregnancy. Female mice previously infected with B. microti gained more weight over pregnancy, and spent more time nursing their offspring. These offspring generated an accelerated response to B. microti as adults, clearing the infection sooner and losing less weight as a result of infection. They also showed an altered hormonal response to novel social environments, decreasing instead of increasing testosterone production upon social housing. These results suggest that a dominance-resistance trade-off can be mediated by cues from the previous generation. We suggest that strategic maternal investment in response to an infection leads to increased disease resistance in the following generation. Offspring from previously infected mothers downregulate investment in acquisition of social dominance, which in natural systems would reduce access to mating opportunities. In doing so, however, they avoid the reduced disease resistance associated with increased testosterone and dominance. The benefits of accelerated clearance of infection and reduced weight loss during infection may outweigh costs associated with reduced social dominance in an environment where the risk of disease is high.

show abstract

Section: Discussionmentioning

confidence: 54%

Section: Introductionmentioning

confidence: 99%

Infection before pregnancy affects immunity and response to social challenge in the next generation

Curno

Reader

McElligott

et al. 2011

Phil. Trans. R. Soc. B

View full text Add to dashboard Cite

show abstract

“…This is an experimental proof that transgenerational transmission of IGT may also occur through the paternal lineage, besides the more widely accepted maternal and grand maternal inheritance of diabetes (Zambrano et al, 2005;Drake et al, 2005;Blondeau et al, 2002;Benyshek et al, 2006). Conceptually, transgenerational inheritance of disease risk may be mediated by nongenomic mechanisms, including either 1) epigenetic mechanisms (Ozanne & Constancia, 2007;Pinney & Simmons, 2009;Drake & Liu, 2009;Waterland & Michels, 2007) or 2) other broader indirect mechanisms associated with parental physiology (Gluckman et al, 2007). First, alterations in nutrition during development can alter epigenetic marks, thus regulating gene expression through DNA methylation and/or histone modifications.…”

Section: Transgenerational Inheritance Of Beta-cell Mass Programmingmentioning

confidence: 79%

Impact and Mechanisms of Pancreatic Beta-Cell Mass Programming by Maternal Diabetes - Insight from Animal Model Studies

Chavey¹,

Movassat²,

Portha³

2011

Gestational Diabetes

View full text Add to dashboard Cite

“…Evidence both from human and animal studies suggests that fetal programming may not be limited to the directly exposed F1 but may be transmitted to subsequent generations without re-exposure (Jimenez-Chillaron et al, 2009;Drake & Liu, 2010). These effects may be transmissible through both maternal and paternal lines (Jimenez-Chillaron et al; Pentinat et al, 2010;Dunn & Bale, 2011).…”

Section: Discussionmentioning

confidence: 99%

Both Hepatic Lipogenesis and Beta-Oxidation are Altered in Offspring of Mothers Fed a High-Fat Diet in the First Two Generations (F1 and F2)

et al. 2015

View full text Add to dashboard Cite

SUMMARY:The high fat (HF) fed mothers may program susceptibility in offspring to chronic diseases and affect subsequent generations. The present study evaluated the liver structure in adulthood, focusing on the F1 and F2 generations. Females C57BL/6 (F0) were fed standard chow (SC) or HF diet (8 weeks) prior to mating and during the gestation and lactation to provide the F1 generation (SC-F1 and HF-F1). All other mothers and offspring fed SC. At 3 months old, F1 females were mated to produce the F2 generation (SC-F2 and HF-F2). The liver was kept in several fragments and prepared for histological analysis or frozen for biochemical and molecular analyzes. The F1 and F2 offspring were studied at 3 months old. HF-F1 had higher body mass (BM) compared to SC-F1 (P= 0.001), but not HF-F2 compared to SC-F2. HF-F1 had glucose intolerance when compared to SC-F1, but not HF-F2 compared to SC-F2. HF-F1 (P= 0.009) and HF-F2 (P= 0.03) showed hyperinsulinemia compared to their counterparts. Both groups HF-F1 and HF-F2 showed more steatosis than the SC counterparts (F1 and F2, P<0.0001). HF-F1 showed increased expression of PPAR-gamma and SREBP1-c compared to SC-F1 (P= 0.01). HF-F2 showed increased PPAR-gamma expression compared to SC-F2 (P= 0.04). In conclusion, HF-fed mother impairs both lipogenesis and beta-oxidation pathways in F1 through upregulation of PPAR-gamma and downregulation of PPAR-alpha. In F2, the only lipogenesis is enhanced, but it causes a disrupted PPAR balance, favoring the hepatic lipid accumulation and impaired metabolism in these animals that were not directly exposed to the maternal HF intake.

show abstract

Intergenerational transmission of programmed effects: public health consequences

Cited by 95 publications

References 86 publications

Infection before pregnancy affects immunity and response to social challenge in the next generation

Infection before pregnancy affects immunity and response to social challenge in the next generation

Impact and Mechanisms of Pancreatic Beta-Cell Mass Programming by Maternal Diabetes - Insight from Animal Model Studies

Both Hepatic Lipogenesis and Beta-Oxidation are Altered in Offspring of Mothers Fed a High-Fat Diet in the First Two Generations (F1 and F2)

Contact Info

Product

Resources

About