Project description:Objective Recent evidence indicates that the adult hematopoietic system is susceptible to diet-induced lineage skewing. It is not known whether the developing hematopoietic system is subject to metabolic programming via in utero high fat diet (HFD) exposure, an established mechanism of adult disease in several organ systems. We previously reported substantial losses in offspring liver size with prenatal HFD. As the liver is the main hematopoietic organ in the fetus, we asked whether the developmental expansion of the hematopoietic stem and progenitor cell (HSPC) pool is compromised by prenatal HFD and/or maternal obesity. Methods We used quantitative assays, progenitor colony formation, flow cytometry, transplantation, and gene expression assays with a series of dietary manipulations to test the effects of gestational high fat diet and maternal obesity on the day 14.5 fetal liver hematopoietic system. Results Maternal obesity, particularly when paired with gestational HFD, restricts physiological expansion of fetal HSPCs while promoting the opposing cell fate of differentiation. Importantly, these effects are only partially ameliorated by gestational dietary adjustments for obese dams. Competitive transplantation reveals compromised repopulation and myeloid-biased differentiation of HFD-programmed HSPCs to be a niche-dependent defect, apparent in HFD-conditioned male recipients. Fetal HSPC deficiencies coincide with perturbations in genes regulating metabolism, immune and inflammatory processes, and stress response, along with downregulation of genes critical for hematopoietic stem cell self-renewal and activation of pathways regulating cell migration. Conclusions Our data reveal a previously unrecognized susceptibility to nutritional and metabolic developmental programming in the fetal HSPC compartment, which is a partially reversible and microenvironment-dependent defect perturbing stem and progenitor cell expansion and hematopoietic lineage commitment. Examination of differentially expressed genes between gestational day 15 (+/- 0.5 days) C57BL/6 mouse fetal livers from diet-induced (60% fat diet) obese or control female mice.

Project description:OBJECTIVE:Recent evidence indicates that the adult hematopoietic system is susceptible to diet-induced lineage skewing. It is not known whether the developing hematopoietic system is subject to metabolic programming via in utero high-fat diet (HFD) exposure, an established mechanism of adult disease in several organ systems. We previously reported substantial losses in offspring liver size with prenatal HFD. As the liver is the main hematopoietic organ in the fetus, we asked whether the developmental expansion of the hematopoietic stem and progenitor cell (HSPC) pool is compromised by prenatal HFD and/or maternal obesity. METHODS:We used quantitative assays, progenitor colony formation, flow cytometry, transplantation, and gene expression assays with a series of dietary manipulations to test the effects of gestational high-fat diet and maternal obesity on the day 14.5 fetal liver hematopoietic system. RESULTS:Maternal obesity, particularly when paired with gestational HFD, restricts physiological expansion of fetal HSPCs while promoting the opposing cell fate of differentiation. Importantly, these effects are only partially ameliorated by gestational dietary adjustments for obese dams. Competitive transplantation reveals compromised repopulation and myeloid-biased differentiation of HFD-programmed HSPCs to be a niche-dependent defect, apparent in HFD-conditioned male recipients. Fetal HSPC deficiencies coincide with perturbations in genes regulating metabolism, immune and inflammatory processes, and stress response, along with downregulation of genes critical for hematopoietic stem cell self-renewal and activation of pathways regulating cell migration. CONCLUSIONS:Our data reveal a previously unrecognized susceptibility to nutritional and metabolic developmental programming in the fetal HSPC compartment, which is a partially reversible and microenvironment-dependent defect perturbing stem and progenitor cell expansion and hematopoietic lineage commitment.

Project description:OBJECTIVE:We examined whether the role of maternal education in children's unhealthy snacking diet is moderated by other socio-economic indicators. METHODS:Participants were selected from the Amsterdam Born Children and their Development cohort, a large ongoing community-based birth cohort. Validated Food Frequency Questionnaires (FFQ) (n = 2782) were filled in by mothers of children aged 5.7±0.5yrs. Based on these FFQs, a snacking dietary pattern was derived using Principal Component Analysis. Socio-economic indicators were: maternal and paternal education (low, middle, high; based on the highest education completed) household finance (low, high; based on ability to save money) and neighbourhood SES (composite score including educational level, household income and employment status of residents per postal code). Cross-sectional multivariable linear regression analysis was used to assess the association and possible moderation of maternal education and other socio-economic indicators on the snacking pattern score. Analyses were adjusted for children's age, sex and ethnicity. RESULTS:Low maternal education (B 0.95, 95% CI 0.83;1.06), low paternal education (B 0.36, 95% CI 0.20;0.52), lower household finance (B 0.18, 95% CI 0.11;0.26) and neighbourhood SES (B -0.09, 95% CI -0.11;-0.06) were independently associated with higher snacking pattern scores (p<0.001). The association between maternal education and the snacking pattern score was somewhat moderated by household finance (p = 0.089) but remained strong. Children from middle-high educated mothers (B 0.44, 95% CI 0.35;0.52) had higher snacking pattern scores when household finance was low (B 0.49, 95% CI 0.33;0.65). CONCLUSIONS:All socio-economic indicators were associated with increased risk of unhealthy dietary patterns in young children, with low maternal education conferring the highest risk. Yet, within the group of middle-high educated mothers, lower household finance was an extra risk factor for unhealthy dietary patterns. Intervention strategies should therefore focus on lower educated mothers and middle-high educated mothers with insufficient levels of household finance.

Project description:Objective Recent evidence indicates that the adult hematopoietic system is susceptible to diet-induced lineage skewing. It is not known whether the developing hematopoietic system is subject to metabolic programming via in utero high fat diet (HFD) exposure, an established mechanism of adult disease in several organ systems. We previously reported substantial losses in offspring liver size with prenatal HFD. As the liver is the main hematopoietic organ in the fetus, we asked whether the developmental expansion of the hematopoietic stem and progenitor cell (HSPC) pool is compromised by prenatal HFD and/or maternal obesity. Methods We used quantitative assays, progenitor colony formation, flow cytometry, transplantation, and gene expression assays with a series of dietary manipulations to test the effects of gestational high fat diet and maternal obesity on the day 14.5 fetal liver hematopoietic system. Results Maternal obesity, particularly when paired with gestational HFD, restricts physiological expansion of fetal HSPCs while promoting the opposing cell fate of differentiation. Importantly, these effects are only partially ameliorated by gestational dietary adjustments for obese dams. Competitive transplantation reveals compromised repopulation and myeloid-biased differentiation of HFD-programmed HSPCs to be a niche-dependent defect, apparent in HFD-conditioned male recipients. Fetal HSPC deficiencies coincide with perturbations in genes regulating metabolism, immune and inflammatory processes, and stress response, along with downregulation of genes critical for hematopoietic stem cell self-renewal and activation of pathways regulating cell migration. Conclusions Our data reveal a previously unrecognized susceptibility to nutritional and metabolic developmental programming in the fetal HSPC compartment, which is a partially reversible and microenvironment-dependent defect perturbing stem and progenitor cell expansion and hematopoietic lineage commitment.

Project description:Aims:Obesity during pregnancy increases risk of cardiovascular disease (CVD) in the offspring and individuals exposed to over-nutrition during fetal life are likely to be exposed to a calorie-rich environment postnatally. Here, we established the consequences of combined exposure to a maternal and post-weaning obesogenic diet on offspring cardiac structure and function using an established mouse model of maternal diet-induced obesity. Methods and results:The impact of the maternal and postnatal environment on the offspring metabolic profile, arterial blood pressure, cardiac structure, and function was assessed in 8-week-old C57BL/6 male mice. Measurement of cardiomyocyte cell area, the transcriptional re-activation of cardiac fetal genes as well as genes involved in the regulation of contractile function and matrix remodelling in the adult heart were determined as potential mediators of effects on cardiac function. In the adult offspring: a post-weaning obesogenic diet coupled with exposure to maternal obesity increased serum insulin (P?<?0.0001) and leptin levels (P?<?0.0001); maternal obesity (P?=?0.001) and a post-weaning obesogenic diet (P?=?0.002) increased absolute heart weight; maternal obesity (P?=?0.01) and offspring obesity (P?=?0.01) caused cardiac dysfunction but effects were not additive; cardiac dysfunction resulting from maternal obesity was associated with re-expression of cardiac fetal genes (Myh7: Myh6 ratio; P?=?0.0004), however, these genes were not affected by offspring diet; maternal obesity (P?=?0.02); and offspring obesity (P?=?0.05) caused hypertension and effects were additive. Conclusions:Maternal diet-induced obesity and offspring obesity independently promote cardiac dysfunction and hypertension in adult male progeny. Exposure to maternal obesity alone programmed cardiac dysfunction, associated with hallmarks of pathological left ventricular hypertrophy, including increased cardiomyocyte area, upregulation of fetal genes, and remodelling of cardiac structure. These data highlight that the perinatal period is just as important as adult-onset obesity in predicting CVD risk. Therefore, early developmental periods are key intervention windows to reduce the prevalence of CVD.

Project description:OBJECTIVES:Non-communicable diseases account for 50% of all deaths in Nepal and 25% result from cardiovascular diseases. Previous studies in Nepal indicate a high burden of behavioural cardiovascular risk factors, suggesting a low level of knowledge, attitude and practice/behaviour regarding cardiovascular health. The behavioural foundation for a healthy lifestyle begins in early childhood, when mothers play a key role in their children's lives. This qualitative study, conducted in a Nepalese peri-urban community, aimed to explore mothers' perception of their children's diet and physical activity. DESIGN:We notated, tape-recorded and transcribed all data collected from six focus group discussions, and used qualitative content analysis for evaluation and interpretation. SETTING:The study was conducted in the Jhaukhel-Duwakot Health Demographic Surveillance Site in the Bhaktapur district of Nepal. PARTICIPANTS:Local health workers helped recruit 61 women with children aged 5-10?years. We distributed participants among six different groups according to educational status. RESULTS:Although participants understood the importance of healthy food, they misunderstood its composition, perceiving it as unappetising and appropriate only for sick people. Furthermore, participants did not prioritise their children's physical activities. Moreover, mothers believed they had limited control over their children's dietary habits and physical activity. Finally, they opined that health educational programmes would help mothers and recommended various intervention strategies to increase knowledge regarding a healthy lifestyle. CONCLUSIONS:Our data reveal that mothers of young children in a peri-urban community of Nepal lack adequate and accurate understanding about the impact of a healthy diet and physical activity. Therefore, to prevent future cardiovascular disease and other non-communicable diseases among children, Nepal needs health education programmes to improve mothers' cardiovascular health knowledge, attitude and behaviour.

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Maternal work and children's diet, activity, and obesity.

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Maternal work and children's diet, activity, and obesity.

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