Glucose metabolism is altered in the adequately-nourished grand-offspring (F3 generation) of rats malnourished during gestation and perinatal life

Benyshek, Daniel C.; Johnston, Carol S.; Martin, John F.

doi:10.1007/s00125-006-0196-5

Cited by 196 publications

(140 citation statements)

References 6 publications

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“…Insulin sensitivity was significantly reduced in all F2 animals versus control animal. However insulin resistance was not dependent on offspring birthweight and persisted regardless of dietary treatment [89].…”

Section: Alleviating Malprogramming By Diet or Drug?mentioning

confidence: 87%

“…This beta-cell alteration was also present in the next generation [91]. Glucose metabolism was shown to be altered in the adequately nourished offspring of the offspring of rats malnourished (LPD) during gestation and perinatal life, demonstrating the persistence of the effects in the third generation [89]. Undernourishment in utero produces striking insulin resistance in genetically normal, wellnourished second-generation rats.…”

Section: Effects Present In the F1 Persisting To The F2 And Beyondmentioning

confidence: 92%

“…Accordingly it must be stressed that in some cases of maintenance of trait to F2, such cases can derive from direct exposure of F1 fetal gonadal cells via exposure of the F0 gestating female [88]. However, as previously described above, through a vicious cycle of mother-tooffspring transmission, iterative somatic alterations occurring in the womb and/or in the postnatal period under the influence of social, metabolic, nutritional or toxicological environmental factors do represent TGEs that do not necessarily affect the germline [34, 89,90].…”

Section: Continuous/discrete Exposure To the Initial Stimulus And Permentioning

confidence: 99%

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Sexual dimorphism in environmental epigenetic programming

Gabory

Attig

Junien

2009

Molecular and Cellular Endocrinology

246

196

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The phenotype of an individual is the result of complex interactions between genotype and current, past and ancestral environment leading to a lifelong remodelling of our epigenomes. The vast majority of common diseases, including atherosclerosis, diabetes, osteoporosis, asthma, neuropsychological and autoimmune diseases, which often take root in early development, display some degree of sex bias, very marked in some cases. This bias could be explained by the role of sex chromosomes, the different regulatory pathways underlying sexual development of most organs and finally, lifelong fluctuating impact of sex hormones. A substantial proportion of dimorphic genes expression might be under the control of sex-specific epigenetic marks. Environmental factors such as social behaviour, nutrition or chemical compounds can influence, in a gender-related manner, these flexible epigenetic marks during particular spatiotemporal windows of life. Thus, finely tuned developmental program aspects, for each sex, may be more sensitive to specific environmental challenges, particularly during developmental programming and gametogenesis, but also throughout the individual's life under the influence of sex steroid hormones and/or sex chromosomes. An unfavourable programming could thus lead to various defects and different susceptibility to diseases between males and females. Recent studies suggest that this epigenetic programming could be sometimes transmitted to subsequent generations in a sex specific manner and lead to transgenerational effects (TGEs).This review summarizes the current understanding in the field of epigenetic programming and highlights the importance of studying both sexes in epidemiological protocols or dietary interventions both in humans and in experimental animal models.

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Section: Alleviating Malprogramming By Diet or Drug?mentioning

confidence: 87%

Section: Effects Present In the F1 Persisting To The F2 And Beyondmentioning

confidence: 92%

Section: Continuous/discrete Exposure To the Initial Stimulus And Permentioning

confidence: 99%

See 1 more Smart Citation

Sexual dimorphism in environmental epigenetic programming

Gabory

Attig

Junien

2009

Molecular and Cellular Endocrinology

246

196

View full text Add to dashboard Cite

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“…Importantly, not only maternal but also certain paternal environmental exposure might induce epigenetic modifications. The findings supporting true transgenerational inheritance (F3) include altered glucose metabolism in F3 descending from rats (F0) on protein-restricted diet, 99 and increased female body size in F3 from F0 mice on maternal high-fat diet, an effect that was perpetuated paternally. 100 In man, information from prepubertal nutritional state has been reported to be transmitted through the germ-line affecting cardiovascular and diabetes mortality two generations later (F2).…”

Section: Transgenerational Inheritance Of Epigenetic Patternsmentioning

confidence: 89%

Epigenetic regulation in obesity

2011

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The availability to the DNA strand and the activity of the transcription machinery is crucial for the cell to use the information in the DNA. The epigenetic mechanisms DNA methylation, modification of histone tails, other chromatin-modifying processes and interference by small RNAs regulate the cell-type-specific DNA expression. Epigenetic marks can be more or less plastic perpetuating responses to various molecular signals and environmental stimuli, but in addition apparently stochastic epigenetic marks have been found. There is substantial evidence from animal and man demonstrating that both transient and more long-term epigenetic mechanisms have a role in the regulation of the molecular events governing adipogenesis and glucose homeostasis. Intrauterine exposure such as poor maternal nutrition has consistently been demonstrated to contribute to a particular epigenotype and thereby developmental metabolic priming of the exposed offspring in animal and man. Epigenetic modifications can be passed not only from one cell generation to the next, but metabolic disease-related epigenotypes have been proposed to also be transmitted germ-line. Future more comprehensive knowledge on epigenetic regulation will complement genome sequence data for the understanding of the complex etiology of obesity and related disorder.

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“…Recent research in human and animal models suggests that biological adaptations to environmental exposures during critical or sensitive periods of development may be transmitted to subsequent generations (Benyshek 2013), such that a trait like insulin resistance in the exposed generation might be passed to successive unexposed generations in diminishing order of magnitude (Benyshek et al 2006). This transgenerational transmission goes beyond something that might be explained by genetic heritability or by family members of different generations experiencing similar lifelong environments.…”

Section: Transgenerational Transmissionmentioning

confidence: 99%