Maternal over-nutrition and offspring obesity predisposition: targets for preventative interventions

Rooney, Kieron; Ozanne, Susan E.

doi:10.1038/ijo.2011.96

Cited by 89 publications

(74 citation statements)

References 66 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The precise obesogenic environmental factors that mediate these effects are not known. 28 Third, although the plots in Figure 1 show a significant and positive association between maternal adiposity measures and neonatal skin fold thickness, the range is quite wide across the x axis, suggesting that the amount and distribution of fat stores in the neonate may reflect other important factors that we have not examined in this paper but would be important to explore further. Such factors include maternal nutritional status before pregnancy, perinatal nutritional status of the neonate and genetic and epigenetic changes that can cross from generation to generation but have yet to be fully explored and remain an important focus of current and future research in this area.…”

Section: Discussionmentioning

confidence: 89%

Maternal and infant factors associated with neonatal adiposity: Results from the Tasmanian Infant Health Survey (TIHS)

et al. 2012

View full text Add to dashboard Cite

OBJECTIVE:To examine the maternal and neonatal factors associated with offspring adiposity and the role of birth and placental weight as potential mediators in such associations. DESIGN: The Tasmanian Infant Health Survey was a prospective cohort study conducted between 1988 and 1995 in Australia to investigate the cause of Sudden Infant Death Syndrome. This large infant cohort provides measurement of skinfolds on 7945 mothers and their offspring. SUBJECTS: Participants included singletons born X37 weeks gestation who were at high risk of sudden infant death syndrome identified through a composite score that included birth weight, maternal age, neonatal gender, season of birth, duration of second-stage labor and intention to breastfeed. MEASUREMENTS: Neonatal adiposity was assessed from skinfold measurements of the subscapular (SSF) and triceps folds (TSF) taken at birth. Maternal early-pregnancy body mass index (BMI) was calculated from self-reported height and weight. Neonatal data were extracted from birth records. Data relating to other environmental exposures were obtained from questionnaires administered when neonates were B4-days old. RESULTS: In multivariable models, higher maternal adiposity, increasing maternal age, gestation age, delivery by Caesarian section and female gender were associated with larger SSF independent of placental and birth weight (Po0.001). Maternal age and delivery by Caesarian section were significantly associated with larger TSF, whereas gestational age and male gender were associated with thinner TSF independent of placental and birth weight. Higher early-pregnancy BMI, maternal weight gain, maternal age, parity and gestational age were significantly associated with larger placental and birth weight. Smoking during pregnancy was associated with smaller birth weight but not with placental weight. CONCLUSION: In addition to birth weight, maternal adiposity and placental weight were important additional factors associated with neonatal adiposity.

show abstract

Section: Discussionmentioning

confidence: 89%

Maternal and infant factors associated with neonatal adiposity: Results from the Tasmanian Infant Health Survey (TIHS)

et al. 2012

View full text Add to dashboard Cite

show abstract

“…In fact, it has been postulated that it is not dietary fat but maternal adiposity which induces hyperleptinemia, insulin resistance and increased body weight in offspring that persists into adulthood (White et al, 2009). Accoding to this hypothesis, maternal hyperglycemia, hyperinsulinemia, hyperleptinemia and inflammation would be potential mediator candidates (Rooney and Ozanne, 2011).…”

Section: Hypercaloric and High-fat Dietsmentioning

confidence: 99%

Dietary factors, epigenetic modifications and obesity outcomes: Progresses and perspectives

Milagro

Mansego

Miguel

et al. 2013

Molecular Aspects of Medicine

257

161

View full text Add to dashboard Cite

Nutritional factors play a life-long role in human health. Indeed, there is growing evidence that one of the mechanisms by which nutrients and bioactive compounds affect metabolic traits is epigenetics. Complex interactions among food components and histone modifications, DNA methylation, non-coding RNA expression and chromatin remodeling factors lead to a dynamic regulation of gene expression that controls the cellular phenotype. Although perinatal period is the time of highest phenotypic plasticity, contributing largely to developmental programming, also during adulthood there is evidence about a nutritional influence on epigenetic regulation. Similarly to type 2 diabetes, hypertension, atherosclerosis and other metabolic disorders, obesity predisposition and weight loss outcomes have been repeatedly associated to changes in epigenetic patterns. Different non-nutritional risk factors that usually accompany obesity seem also to be involved in these epigenetic modifications, especially hyperglycemia, inflammation, hypoxia and oxidative stress. There are currently three major objectives in epigenetic research in relation to obesity: to search for epigenetic biomarkers to predict future health problems or detect the individuals at most risk, to understand the obesity-related environmental factors that could modulate gene expression by affecting epigenetic mechanisms, and to study novel therapeutic strategies based on nutritional or pharmacological agents that can modify epigenetic marks. At this level, the major tasks are: development of robust epigenetic biomarkers of weight regulation, description of those epigenetic marks more susceptible to be modified by dietary exposures, identification of the active ingredients (and the doses) that alter the epigenome, assessment of the real importance of other obesity-related factors on epigenetic regulation, determination of the period of life in which best results are obtained, and understanding of the importance of the inheritance of these epigenetic marks.

show abstract

“…Concomitant with the rise in obesity is an increase in the number of reproductive-aged women that are overweight or obese (Flegal et al 2010(Flegal et al , 2012. Maternal obesity is a major obstetric risk factor for adverse fetal, neonatal, and maternal outcomes (Leddy et al 2008, Gaillard et al 2013, Mission et al 2013, in addition it has been associated with childhood obesity of offspring (Poston 2012) and an increased risk of those offspring developing the metabolic syndrome during adulthood (Rooney & Ozanne 2011, Frias & Grove 2012. Excessive gestational weight gain (Boynton-Jarrett et al 2011, Deardorff et al 2013) and a pre-pregnancy BMI of overweight/obese (Keim et al 2009, Deardorff et al 2013 are associated with early menarche in humans; however, childhood obesity, which is strongly associated with maternal obesity (Catalano et al 2009), is also associated with early menarche (Kaplowitz 2008) making it difficult to ascertain independent effects.…”

Section: Nutrient Excessmentioning

confidence: 99%

Early-life nutritional effects on the female reproductive system

Chan

Tsoulis

Sloboda³

2014

Journal of Endocrinology

View full text Add to dashboard Cite

There is now considerable epidemiological and experimental evidence indicating that early-life environmental conditions, including nutrition, affect subsequent development in later life. These conditions induce highly integrated responses in endocrine-related homeostasis, resulting in persistent changes in the developmental trajectory producing an altered adult phenotype. Early-life events trigger processes that prepare the individual for particular circumstances that are anticipated in the postnatal environment. However, where the intrauterine and postnatal environments differ markedly, such modifications to the developmental trajectory may prove maladaptive in later life. Reproductive maturation and function are similarly influenced by early-life events. This should not be surprising, because the primordial follicle pool is established early in life and is thus vulnerable to early-life events. Results of clinical and experimental studies have indicated that early-life adversity is associated with a decline in ovarian follicular reserve, changes in ovulation rates, and altered age at onset of puberty. However, the underlying mechanisms regulating the relationship between the early-life developmental environment and postnatal reproductive development and function are unclear. This review examines the evidence linking early-life nutrition and effects on the female reproductive system, bringing together clinical observations in humans and experimental data from targeted animal models.

show abstract

Maternal over-nutrition and offspring obesity predisposition: targets for preventative interventions

Cited by 89 publications

References 66 publications

Maternal and infant factors associated with neonatal adiposity: Results from the Tasmanian Infant Health Survey (TIHS)

Maternal and infant factors associated with neonatal adiposity: Results from the Tasmanian Infant Health Survey (TIHS)

Dietary factors, epigenetic modifications and obesity outcomes: Progresses and perspectives

Early-life nutritional effects on the female reproductive system

Contact Info

Product

Resources

About