Hyperlipidic hypercholesterolemic diet in prepubertal rabbits affects gene expression in the embryo, restricts fetal growth and increases offspring susceptibility to obesity

Picone, Olivier; Laigre, P.; Fortun-Lamothe, Laurence; Archilla, Catherine; Peynot, Nathalie; Ponter, Andrew; Berthelot, Valérie; Cordier, Anne; Duranthon, Véronique; Chavatte‐Palmer, Pascale

doi:10.1016/j.theriogenology.2010.08.015

Cited by 66 publications

(93 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Their fertility and prolificacy did not appear to be affected. Even if the target of our study was not to examine reproductive phenomena in detail, fetal intra-uterine growth retardation was observed, despite a similar placental weight, thus illustrating a possible decrease in placental efficiency in OD rabbits (Picone et al, 2011). These observations are in agreement with similar reports on different species in which obesity led to low birth weight (Rolls et al, 1984;Flint et al, 2005).…”

Section: Discussionsupporting

confidence: 88%

An obesogenic diet started before puberty leads to abnormal mammary gland development during pregnancy in the rabbit

Hue-Beauvais¹,

Chavatte‐Palmer

Aujean³

et al. 2011

Developmental Dynamics

View full text Add to dashboard Cite

Alterations to the metabolic environment during puberty can impact future lactation efficiency and mammary tumorigenesis. During this study, we used a model of rabbits receiving an obesogenic diet (OD), starting before puberty and extending until mid-pregnancy. Three months later, the body weight of OD animals was significantly higher than that of controls and their mammary glands displayed a precocious and abnormal development at mid-pregnancy. OD mammary ducts were filled with dense products, while alveolar structures invaded most of the fat pad. The proportion of secretory epithelium was significantly higher in OD mammary tissue, which contained an abundant accumulation of milk proteins and lipids. In conclusion, an obesogenic diet started before puberty induced an accelerated development of the rabbit mammary gland, leading to an accumulation of secretory products at mid-pregnancy. These results support the critical influence of nutrition on mammary growth and differentiation, which may be deleterious to mammary development and subsequent lactation. Developmental Dynamics 240:347-356,

show abstract

Section: Discussionsupporting

confidence: 88%

An obesogenic diet started before puberty leads to abnormal mammary gland development during pregnancy in the rabbit

Hue-Beauvais¹,

Chavatte‐Palmer

Aujean³

et al. 2011

Developmental Dynamics

View full text Add to dashboard Cite

show abstract

“…ebi.ac.uk/ena/data/view). A microarray dedicated to the embryo, although limited in size, has successfully been used to analyze gene expression in the early embryo (Leandri et al 2009) and effects of the embryo's environment (Picone et al 2011). More recently, a larger array has been made commercially available (Agilent Technologies, Palo Alto, CA, USA).…”

Section: Discussionmentioning

confidence: 99%

“…Maternal hypercholesterolemia is also associated with IUGR in rabbits (Montoudis et al 1999) and affects placental transfer of fatty acids and GLUT expression in the placenta (Kevorkova et al 2007, Marseille-Tremblay et al 2007, Ethier-Chiasson et al 2008. When the high-cholesterol diet is enriched with poly-unsaturated fatty acids and is administered to females prior to puberty, gene expression is altered in the female's embryos, which subsequently develop IUGR leading to overweight in adult offspring (Picone et al 2011). The cellular and molecular mechanisms involved are currently being studied.…”

Section: Maternal Dyslipidemiamentioning

confidence: 99%

See 1 more Smart Citation

Rabbit as a reproductive model for human health

Fischer¹,

Chavatte‐Palmer²,

Viebahn³

et al. 2012

Reproduction

179

149

View full text Add to dashboard Cite

The renaissance of the laboratory rabbit as a reproductive model for human health is closely related to the growing evidence of periconceptional metabolic programming and its determining effects on offspring and adult health. Advantages of rabbit reproduction are the exact timing of fertilization and pregnancy stages, high cell numbers and yield in blastocysts, relatively late implantation at a time when gastrulation is already proceeding, detailed morphologic and molecular knowledge on gastrulation stages, and a hemochorial placenta structured similarly to the human placenta. To understand, for example, the mechanisms of periconceptional programming and its effects on metabolic health in adulthood, these advantages help to elucidate even subtle changes in metabolism and development during the pre-and peri-implantation period and during gastrulation in individual embryos. Gastrulation represents a central turning point in ontogenesis in which a limited number of cells program the development of the three germ layers and, hence, the embryo proper. Newly developed transgenic and molecular tools offer promising chances for further scientific progress to be attained with this reproductive model species.

show abstract

“…The expression of the CD36 fatty acid transporter and the binding protein FABP5 was decreased in the placenta of boys and unaffected in that of girls (Brass et al, 2013). Rabbit females fed a lipid-and cholesterol-enriched diet developed high adiposity and dyslipidaemia and their offspring were overweight at adulthood, which was associated with hypertension (Picone et al, 2011). Interestingly, a specific sexually dimorphic response to maternal diet was observed in the placenta.…”

mentioning

confidence: 98%

Placental contribution to nutritional programming of health and diseases: epigenetics and sexual dimorphism

Tarrade

Panchenko

Junien

et al. 2015

Journal of Experimental Biology

205

149

View full text Add to dashboard Cite

The recent and rapid worldwide increase in non-communicable diseases challenges the assumption that genetic factors are the primary contributors to such diseases. A new concept of the 'developmental origins of health and disease' (DOHaD) is at stake and therefore requires a paradigm shift. Maternal obesity and malnutrition predispose offspring to develop metabolic syndrome, a vicious cycle leading to transmission to subsequent generation(s), with differences in response and susceptibility according to the sex of the individual. The placenta is a programming agent of adult health and disease. Adaptations of placental phenotype in response to maternal diet and metabolic status alter fetal nutrient supply. This implies important epigenetic changes that are, however, still poorly documented in DOHaD studies, particularly concerning overnutrition. The aim of this review is to discuss the emerging knowledge on the relationships between the effect of maternal nutrition or metabolic status on placental function and the risk of diseases later in life, with a specific focus on epigenetic mechanisms and sexual dimorphism. Explaining the sex-specific causal variables and how males versus females respond and adapt to environmental perturbations should help physicians and patients to anticipate disease susceptibility.KEY WORDS: DOHaD, Fetal programming, Placenta, Sex, Nutrition, Obesity, Maternal environment, Gestation Introduction: developmental origins of health and diseaseThe recent and rapid worldwide increase in non-communicable diseases (NCDs) challenges the assumption that genetic factors are the primary contributors to such diseases (McAllister et al., 2009). The 'developmental origins of health and disease' (DOHaD) paradigm states that the environment during the periconception, gestation and lactation periods shapes the developing individuals, leading, in the case of a deleterious environment, to a predisposition to adult-onset diseases. This theory was popularised by D. J. Barker in the early 1990s (Barker, 1990) but the question had already been raised in earlier studies. In the 1960s and 1970s, different experiments on diverse mammalian species (rat, mouse, guinea pig, pig, etc.) showed that a reduction of maternal calorie or protein intake during pregnancy and lactation affects the growth capacity and cognitive ability of the offspring (reviewed in Roeder and Chow, 1972;McCance, 1976). Later, this concept was extended to phenotype in general, with a strong implication for quantitative traits in agriculture. An increasing number of studies pointed to the fact that maternal environment in cattle was an important parameter to fully express the genetically highly selected potential of the animals (Wallace et al., 2010; Jammes et al., 2011;Tanghe et al., 2014).Male and female susceptibility to NCDs is well described. It appears that in the DOHaD context, the same environmental exposure may affect the long-term health of the offspring with a discrepancy between males and females in terms of the timing, onset ...

show abstract

Hyperlipidic hypercholesterolemic diet in prepubertal rabbits affects gene expression in the embryo, restricts fetal growth and increases offspring susceptibility to obesity

Cited by 66 publications

References 48 publications

An obesogenic diet started before puberty leads to abnormal mammary gland development during pregnancy in the rabbit

An obesogenic diet started before puberty leads to abnormal mammary gland development during pregnancy in the rabbit

Rabbit as a reproductive model for human health

Placental contribution to nutritional programming of health and diseases: epigenetics and sexual dimorphism

Contact Info

Product

Resources

About