Offspring Fat Mass Research Articles

Maternal plasma polyunsaturated fatty acid status in late pregnancy is associated with offspring body composition in childhood.

Maternal diet during pregnancy has been linked to offspring adiposity, but it is unclear whether maternal polyunsaturated fatty acid (PUFA) status during pregnancy affects offspring body composition. We investigated the associations between maternal plasma n-3 and n-6 PUFA status at 34 wk gestation and offspring body composition. A prospective United Kingdom population-based mother-offspring cohort, the Southampton Women's Survey (SWS), was studied. A total of 12,583 nonpregnant women were recruited into the SWS, among whom 1987 delivered a baby before December 31, 2003; 293 mother-child pairs had complete measurements of maternal plasma PUFA concentrations in late pregnancy and offspring body composition at both ages 4 and 6 yr. We measured offspring body composition by dual-energy x-ray absorptiometry, yielding fat mass, lean mass, percentage fat mass, and percentage lean mass. Results are presented as β-coefficients for standardized variables, therefore reflecting the sd change of the outcome for every 1 sd of the predictor. After adjustment for maternal factors and child factors including height and duration of breast-feeding, maternal plasma n-6 PUFA concentration positively predicted offspring fat mass at 4 yr (β = 0.14 SD/SD; P = 0.01) and 6 yr (β = 0.11 SD/SD; P = 0.04), but there was no association with offspring lean mass at either age (β = 0.005 SD/SD, P = 0.89; and β = 0.008 SD/SD, P = 0.81, respectively). Maternal plasma n-3 PUFA concentration was not associated with offspring fat mass at 4 yr (β = 0.057 SD/SD; P = 0.34) or 6 yr (β = 0.069 SD/SD; P = 0.21). Maternal plasma n-3 PUFA status was positively associated with offspring lean mass on univariate analysis (4 yr, β = 0.11, P = 0.06; 6 yr, β = 0.14; P = 0.02); however, this was confounded by a positive association with offspring height. This observational study suggests that maternal n-6 PUFA status during pregnancy might influence offspring adiposity in childhood.

Maternal diet, breastfeeding and adolescent body composition: a 16-year prospective study

Overweight and obesity are becoming increasingly prevalent problems worldwide. A number of factors in early life have been found to be associated with body composition of neonates or young children but there is limited follow-up data for adolescents. This study aims to describe associations between early nutrition and body composition in adolescents. Birth cohort study of 415 pregnant women and their offspring (mean age 16 years). Body composition including fat mass (FM) and lean body mass (LBM) of adolescents at 16 years of age was measured by dual-energy X-ray absorptiometry. Information on maternal food and nutrients intake during the third trimester of pregnancy and breastfeeding was collected by questionnaires soon after birth. A total of 264 mother-adolescents pairs were studied. Maternal antenatal meat intake was positively associated with FM of adolescents (an increase of 0.9%/portion, P<0.01). There were also positive associations between maternal energy intake (per 1000 kJ/day), fat (per 10 g/d) and protein (per 10 g/day) intake and offspring's FM (an increase of 1.3%), but these became borderline after adjustment for confounders. Breastfeeding >25 days was negatively associated with FM in adolescents (a decrease of 14%, P=0.01). These associations were independent of the significant association between maternal energy and macronutrient intakes during pregnancy and adolescent intakes at 16 years of age. No significant association was found between maternal dietary intake and lean mass in adolescents. Breastfeeding may have a biological effect that is beneficial for the prevention of obesity. Conversely, higher maternal meat intake during pregnancy may increase FM in adolescents.

Fetal Liver Blood Flow Distribution: Role in Human Developmental Strategy to Prioritize Fat Deposition versus Brain Development

Among primates, human neonates have the largest brains but also the highest proportion of body fat. If placental nutrient supply is limited, the fetus faces a dilemma: should resources be allocated to brain growth, or to fat deposition for use as a potential postnatal energy reserve? We hypothesised that resolving this dilemma operates at the level of umbilical blood distribution entering the fetal liver. In 381 uncomplicated pregnancies in third trimester, we measured blood flow perfusing the fetal liver, or bypassing it via the ductus venosus to supply the brain and heart using ultrasound techniques. Across the range of fetal growth and independent of the mother's adiposity and parity, greater liver blood flow was associated with greater offspring fat mass measured by dual-energy X-ray absorptiometry, both in the infant at birth (r = 0.43, P<0.001) and at age 4 years (r = 0.16, P = 0.02). In contrast, smaller placentas less able to meet fetal demand for essential nutrients were associated with a brain-sparing flow pattern (r = 0.17, p = 0.02). This flow pattern was also associated with a higher degree of shunting through ductus venosus (P = 0.04). We propose that humans evolved a developmental strategy to prioritize nutrient allocation for prenatal fat deposition when the supply of conditionally essential nutrients requiring hepatic inter-conversion is limited, switching resource allocation to favour the brain if the supply of essential nutrients is limited. Facilitated placental transfer mechanisms for glucose and other nutrients evolved in environments less affluent than those now prevalent in developed populations, and we propose that in circumstances of maternal adiposity and nutrient excess these mechanisms now also lead to prenatal fat deposition. Prenatal developmental influences play important roles in the human propensity to deposit fat.

Maternal vitamin D status in pregnancy is associated with adiposity in the offspring: findings from the Southampton Women’s Survey

Low vitamin D status has been linked to adiposity, but little is known of the effects of low status in pregnancy on offspring body composition. The objective was to determine how maternal vitamin D status relates to lean and fat mass of the offspring. The offspring of 977 pregnant women, who had serum 25-hydroxyvitamin D [25(OH)D] measured at 34 wk gestation, were followed up within 3 wk of birth and at 4 and 6 y of age for dual-energy X-ray absorptiometry assessment of lean and fat mass. The median maternal serum 25(OH)D concentration was 62 nmol/L (IQR: 43-89 nmol/L); 35% of the women studied had values <50 nmol/L. Lower vitamin D status was associated with lower fat mass in the offspring at birth but with greater fat mass at ages 4 and 6 y. It was not associated with lean mass at any of the ages studied. The opposing associations seen between maternal 25(OH)D (SDs) and fat mass (SDs) in the offspring at birth and at age 6 y were robust to adjustment for a range of confounding factors, including maternal BMI and weight gain in pregnancy [β (95% CI): 0.08 (0.02, 0.15) and -0.10 (-0.17, -0.02), respectively]. The key independent predictors of higher maternal vitamin D status were season of assessment and use of vitamin D supplements. Lower maternal vitamin D status may be linked to programmed differences in offspring fat mass. The findings require replication but add to a growing evidence base for a role of vitamin D in the origins of adiposity.

Effect of reducing the n−6:n−3 long-chain PUFA ratio during pregnancy and lactation on infant adipose tissue growth within the first year of life: an open-label randomized controlled trial

The composition of long-chain PUFAs (LCPUFAs) in the maternal diet may affect obesity risk in the mother's offspring. We hypothesized that a reduction in the n-6 (omega-6):n-3 (omega-3) LCPUFA ratio in the diet of pregnant women and breastfeeding mothers may prevent expansive adipose tissue growth in their infants during the first year of life. In a randomized controlled trial, 208 healthy pregnant women were randomly assigned to an intervention (1200 mg n-3 LCPUFAs as a supplement per day and a concomitant reduction in arachidonic acid intake) or a control diet from the 15th wk of pregnancy to 4 mo of lactation. The primary outcome was infant fat mass estimated by skinfold thickness (SFT) measurements at 4 body sites at 3-5 d, 6 wk, and 4 and 12 mo postpartum. Secondary endpoints included sonographic assessment of abdominal subcutaneous and preperitoneal fat, fat distribution, and child growth. Infants did not differ in the sum of their 4 SFTs at ≤1 y of life [intervention: 24.1 ± 4.4 mm (n = 85); control: 24.1 ± 4.1 mm (n = 80); mean difference: -0.0 mm (95% CI: -1.3, 1.3 mm)] or in growth. Likewise, longitudinal ultrasonography showed no significant differences in abdominal fat mass or fat distribution. We showed no evidence that supplementation with n-3 fatty acids and instructions to reduce arachidonic acid intake during pregnancy and lactation relevantly affects fat mass in offspring during the first year of life. Prospective long-term studies are needed to explore the efficacy of this dietary approach for primary prevention. This trial was registered at clinicaltrials.gov as NCT00362089.

The effect of maternal omega-3 long-chain polyunsaturated fatty acid (n-3 LCPUFA) supplementation during pregnancy and/or lactation on body fat mass in the offspring: A systematic review of animal studies

Dietary n-3 long-chain polyunsaturated fatty acids (n-3 LCPUFA) reduce adipogenesis and lipogenesis in adult rodents, but it is not clear whether an increased n-3 LCPUFA supply during the perinatal period influences body fat mass in the offspring. This systematic review aimed to evaluate the existing evidence from animal studies, which have addressed this question. Medline was searched for relevant articles. Studies were included if they involved maternal n-3 PUFA or LCPUFA supplementation and measured fat mass in the offspring. The design and quality of each study was assessed. Only four animal studies met our inclusion criteria. Three studies reported a lower fat mass in offspring of n-3 LCPUFA supplemented dams, however only one of these studies confined the intervention to the perinatal period. The dose of n-3 PUFA, the nature of the control treatment, the approaches used and outcomes assessed differed between studies. This review highlights the paucity of robust animal data as to the effect of increased n-3 LCPUFA exposure during the perinatal period alone, on body fat mass in the offspring and calls for further studies.

Effect of long-chain polyunsaturated fatty acid supplementation during pregnancy or lactation on infant and child body composition: a systematic review

n-3 (omega-3) Long-chain polyunsaturated fatty acids (LC-PUFAs) inhibit fat cell differentiation and fat storage in adults, and this has led to the hypothesis that maternal n-3 LC-PUFA supplementation may reduce fat mass in children. The objective of this systematic review was to evaluate the effect of n-3 LC-PUFA supplementation in pregnancy or lactation on infant and child body composition in randomized controlled trials. MEDLINE and EMBASE databases were searched for relevant articles. Human trials that supplemented the maternal diet with n-3 LC-PUFAs during pregnancy or lactation and assessed either body fat mass or body mass index in children were included. Trials had to be randomized in design. The quality of all included studies was assessed against set criteria, and results of eligible trials were compared. There were only 3 human trials (4 publications) that met our inclusion criteria. There was considerable disparity in study design and trial quality. The results were variable and showed positive, negative, or neutral effects of maternal n-3 LC-PUFA supplementation on body fat mass in children. This systematic review highlights the paucity of robust data from human studies to evaluate the effect of increased n-3 LC-PUFA exposure during the perinatal period on body fat mass in offspring. Further studies are required in which the intervention is confined to the perinatal period and that are sufficiently powered, have appropriate controls, have adequate blinding of participants and investigators, and have high retention rates.

Maternal Overnutrition Impacts Offspring Adiposity and Brain Appetite Markers‐Modulation by Postweaning Diet

Maternal obesity has long-term consequences for the development of hypothalamic neurones involved in energy homeostasis and the metabolic profile in offspring. In the present study, we compared the effects of maternal obesity induced by longstanding high-fat diet (HFD) with milder postnatal overfeeding during suckling induced by litter size reduction. Female Sprague-Dawley rats consumed chow (C) or HFD. On postnatal day 1, litters from chow dams were adjusted to three per dam (small litter, CS) versus 12 control (normal litter, CN). Litters from HFD dams were adjusted to 12 per dam and fed HFD after weaning to induce obesity (HN). Thus, two degrees of maternal overnutrition were produced (CS and HN). To test whether postweaning diet can amplify the effects of maternal obesity, male offspring weaned onto chow or HFD were followed to 21 weeks. Maternal postnatal overnutrition (CS) and HFD-induced maternal obesity (HN) increased body weight and fat mass in offspring compared to those from control dams (CN). Significant glucose intolerance was induced by both degrees of maternal overnutrition, but only in offspring consuming HFD. HFD-induced maternal obesity (HN) was linked to increased offspring leptin, insulin, lipids, insulin resistance and hyperphagia, and was exaggerated by postweaning HFD. No effect of maternal postnatal overnutrition (CS) was seen on these parameters. Hypothalamic signal transducer and activator of transcription-3 and suppressor of cytokine signalling-3 mRNA were significantly elevated by maternal HFD (HN) in the HFD-fed offspring. The data obtained suggest that even mild maternal overnutrition (CS) led to increased adiposity, glucose intolerance and altered brain appetite regulators in offspring. A greater impact of HFD-induced maternal obesity was evident. Marked additive effects were observed when animals consumed a HFD postweaning.

244: Excess weight gain increases neonatal fat mass in women treated for mild gestational diabetes

To evaluate the relationship between pre-pregnancy maternal body mass index (BMI), gestational weight gain (GWG), birthweight, and neonatal fat mass in offspring of women treated for mild gestational diabetes (GDM).

Exploring the developmental overnutrition hypothesis using parental-offspring associations and FTO as an instrumental variable.

BackgroundThe developmental overnutrition hypothesis suggests that greater maternal obesity during pregnancy results in increased offspring adiposity in later life. If true, this would result in the obesity epidemic progressing across generations irrespective of environmental or genetic changes. It is therefore important to robustly test this hypothesis.Methods and FindingsWe explored this hypothesis by comparing the associations of maternal and paternal pre-pregnancy body mass index (BMI) with offspring dual energy X-ray absorptiometry (DXA)–determined fat mass measured at 9 to 11 y (4,091 parent–offspring trios) and by using maternal FTO genotype, controlling for offspring FTO genotype, as an instrument for maternal adiposity. Both maternal and paternal BMI were positively associated with offspring fat mass, but the maternal association effect size was larger than that in the paternal association in all models: mean difference in offspring sex- and age-standardised fat mass z-score per 1 standard deviation BMI 0.24 (95% confidence interval [CI]: 0.22 to 0.26) for maternal BMI versus 0.13 (95% CI: 0.11, 0.15) for paternal BMI; p-value for difference in effect < 0.001. The stronger maternal association was robust to sensitivity analyses assuming levels of non-paternity up to 20%. When maternal FTO, controlling for offspring FTO, was used as an instrument for the effect of maternal adiposity, the mean difference in offspring fat mass z-score per 1 standard deviation maternal BMI was −0.08 (95% CI: −0.56 to 0.41), with no strong statistical evidence that this differed from the observational ordinary least squares analyses (p = 0.17).ConclusionsNeither our parental comparisons nor the use of FTO genotype as an instrumental variable, suggest that greater maternal BMI during offspring development has a marked effect on offspring fat mass at age 9–11 y. Developmental overnutrition related to greater maternal BMI is unlikely to have driven the recent obesity epidemic.

Higher serum insulin level due to greater total body fat mass in offspring of patients with essential hypertension

To determine whether the offspring of hypertensive patients (OHP) might have a higher serum insulin level than offspring of normotensive parents, we studied 152 girls in junior high school, 21 of whom had at least one hypertensive parent. The remaining 131 girls had normotensive parents and served as the controls. After an overnight fast, we measured the subjects' height, body weight, blood pressure and body fat mass, and collected blood for assay of serum immunoreactive insulin (IRI), lipids and apolipoproteins. Despite a similar body mass index, the OHP had a significantly greater body fat mass ( P < 0.05) and % fat mass ( P < 0.05) than the controls. The OHP exhibited a significantly higher serum IRI level than the controls ( P < 0.05), but no differences in blood pressure or serum lipids. In the OHP, % body fat mass was significantly correlated with systolic blood pressure ( P < 0.05), triglyceride ( P < 0.01) and apolipoprotein B ( P < 0.01), not observed in controls. The serum IRI of the OHP, but not that of controls, was significantly correlated with systolic blood pressure ( P < 0.05), serum triglyceride ( P < 0.02) and apolipoprotein B ( P < 0.05). Thus, a higher serum IRI level due to an increase in total body fat mass appears to be an inherited trait that contributes to the development of hypertension and dyslipidemia.