Dataset Information

Effect of Maternal Obesity and Preconceptional Weight Loss on Male and Female Offspring Metabolism and Olfactory Performance in Mice.

ABSTRACT: According to the "developmental origins of health and disease" (DOHaD) concept, maternal obesity predisposes the offspring to non-communicable diseases in adulthood. While a preconceptional weight loss (WL) is recommended for obese women, its benefits on the offspring have been poorly addressed. We evaluated whether preconceptional WL was able to reverse the adverse effects of maternal obesity in a mouse model, exhibiting a modification of foetal growth and of the expression of genes encoding epigenetic modifiers in liver and placenta. We tracked metabolic and olfactory behavioural trajectories of offspring born to control, obese or WL mothers. After weaning, the offspring were either put on a control diet (CD) or a high-fat (HFD). After only few weeks of HFD, the offspring developed obesity, metabolic alterations and olfactory impairments, independently of maternal context. However, male offspring born to obese mother gained even more weight under HFD than their counterparts born to lean mothers. Preconceptional WL normalized the offspring metabolic phenotypes but had unexpected effects on olfactory performance: a reduction in olfactory sensitivity, along with a lack of fasting-induced, olfactory-based motivation. Our results confirm the benefits of maternal preconceptional WL for male offspring metabolic health but highlight some possible adverse outcomes on olfactory-based behaviours.

SUBMITTER: Panchenko PE

PROVIDER: S-EPMC6566604 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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Effect of Maternal Obesity and Preconceptional Weight Loss on Male and Female Offspring Metabolism and Olfactory Performance in Mice.

Panchenko Polina E PE Lacroix Marie-Christine MC Jouin Mélanie M Voisin Sarah S Badonnel Karine K Lemaire Marion M Meunier Nicolas N Safi-Stibler Sofiane S Persuy Marie-Annick MA Jouneau Luc L Durieux Didier D Lecoutre Simon S Jammes Hélène H Rousseau-Ralliard Delphine D Breton Christophe C Junien Claudine C Baly Christine C Gabory Anne A

Nutrients 20190426 5

According to the "developmental origins of health and disease" (DOHaD) concept, maternal obesity predisposes the offspring to non-communicable diseases in adulthood. While a preconceptional weight loss (WL) is recommended for obese women, its benefits on the offspring have been poorly addressed. We evaluated whether preconceptional WL was able to reverse the adverse effects of maternal obesity in a mouse model, exhibiting a modification of foetal growth and of the expression of genes encoding ep ...[more]

PMID: 31035463

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Project description:BackgroundMaternal obesity (MO) impairs maternal and offspring health. Mechanisms and interventions to prevent adverse maternal and offspring outcomes need to be determined. Human studies are confounded by socio-economic status providing the rationale for controlled animal data on effects of maternal exercise (MEx) intervention on maternal (F0) and offspring (F1) outcomes in MO.HypothesisMO produces metabolic and endocrine dysfunction, increases maternal and offspring glucocorticoid exposure, oxidative stress and adverse offspring outcomes by postnatal day (PND) 36. MEx in part prevents these outcomes.MethodsF0 female rats ate either control or obesogenic diet from weaning through lactation. Half of each group wheel ran (from day 90 of life through pregnancy beginning day 120) providing four groups (n=8/group)--(i) controls, (ii) obese, (iii) exercised controls and (iv) exercised obese. After weaning, PND 21, F1 offspring ate a control diet. Metabolic parameters of F0 prepregnancy and end of lactation and F1 offspring at PND 36 were analyzed.ResultsExercise did not change maternal weight. Before breeding, MO elevated F0 glucose, insulin, triglycerides, cholesterol, leptin, fat and oxidative stress. Exercise completely prevented the triglyceride rise and partially increases glucose, insulin, cholesterol and oxidative stress. MO decreased fertility, recovered by exercise. At the end of lactation, exercise returned all metabolic variables except leptin to control levels. Exercise partially prevented MO elevated corticosterone. F1 offspring weights were similar at birth. At PND 36, MO increased F1 male but not female offspring leptin, triglycerides and fat mass. In controls, exercise reduced male and female offspring glucose, prevented the offspring leptin increase and partially the triglyceride rise.ConclusionsMEx before and during pregnancy has beneficial effects on the maternal and offspring metabolism and endocrine function occurring with no weight change in mothers and offspring indicating the importance of body composition rather than weight in evaluations of metabolic status.

Project description:Maternal nutrition during pregnancy influences postnatal life of animals; nevertheless, few studies have investigated its effects on the productive performance and reproductive development of heifers. This study evaluated the performance, reproductive development, and correlation between reproduction × fat thickness and performance × ribeye area (REA) traits of heifers. We also performed an exploratory genomic association during the rearing period in heifers submitted to fetal programming. The study comprised 55 Nellore heifers born to dams exposed to one of the following nutritional planes: control, without protein-energy supplementation; PELT, protein-energy last trimester, protein-energy supplementation offered in the final third of pregnancy; and PEWG, protein-energy whole gestation, protein-energy supplementation upon pregnancy confirmation. Protein-energy supplementation occurred at the level of 0.3% live weight. After weaning, heifers were submitted to periodic evaluations of weight and body composition by ultrasonography. From 12 to 18 months, we evaluated the reproductive tract of heifers to monitor its development for sexual precocity and ovarian follicle population. The treatments had no effect (p > 0.05) on average daily gain; however, the weight of the animals showed a significant difference over time (p = 0.017). No differences were found between treatments for REA, backfat, and rump fat thickness, nor for puberty age, antral follicular count, and other traits related to reproductive tract development (p > 0.05). The correlation analysis between performance traits and REA showed high correlations (r > 0.37) between REA at weaning and year versus weight from weaning until yearling; however, no correlation was found for reproductive development traits versus fat thickness (p > 0.05). The exploratory genomic association study showed one single-nucleotide polymorphism (SNP) for each treatment on an intergenic region for control and PEWG, and the one for PELT on an intronic region of RAPGEF1 gene. Maternal nutrition affected only the weight of the animals throughout the rearing period.

Project description:BackgroundWeight retention between pregnancies is associated with increased risk of perinatal complications, but it is unclear whether there is an association with offspring weight status. This study aimed to determine whether maternal interpregnancy weight change is associated with offspring overweight/obesity, controlling for confounding variables.Subjects/methodsRoutinely collected linked data from perinatal and child datasets, in Flanders, Belgium were used. Women having their first and second live births between 2009-2018 were included. The association between maternal interpregnancy weight change and overweight/obesity in the second child at 2 years was examined by logistical regression models.ResultsA total of 33,172 women were included. 52.7% (n = 17478) had a stable interpregnancy BMI, 24.1% (n = 8024) and 8.5% (n = 2821) had moderate and substantial BMI increases respectively. At 2 years, 91.6% (n = 30383) of the second offspring had a healthy weight, 0.6% (n = 210), 7.0% (n = 2312) and 0.8% (n = 267) were in the underweight, overweight and obesity BMI categories respectively. Multivariate analysis showed no statistical evidence that maternal interpregnancy BMI change is independently associated with overweight/obesity in the second child. The strongest independent factors were the first child (sibling) being in the obesity category at 2 years (odds ratio [OR] 7.2, [95% CI, 5.49-9.45] and being born Large for Gestational Age (LGA) (2.13 [1.92-2.37]). The following variables were also independently associated with the outcome measure: maternal African origin (1.90 [1.59-2.26]), maternal obesity at start of first pregnancy (1.33 [1.16-1.53]), excessive gestational weight gain in the second pregnancy (1.15 [1.04-1.28]), being born after a < 1-year interpregnancy time interval (1.17 [1.05-1.30]) and not being exclusively breastfed at 12 weeks old (1.29 [1.10-1.52]).ConclusionSibling obesity and being born LGA were most strongly independently associated with overweight/obesity at 2 years. This supports the need for family interventions and to address risk factors for development of LGA infants. There was no independent association with interpregnancy weight gain, contrary to what was hypothesised.

Dataset Information

Effect of Maternal Obesity and Preconceptional Weight Loss on Male and Female Offspring Metabolism and Olfactory Performance in Mice.

Publications

Effect of Maternal Obesity and Preconceptional Weight Loss on Male and Female Offspring Metabolism and Olfactory Performance in Mice.

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