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OBJECTIVE: Physical activity (PA) during pregnancy is associated with lower neonatal fat mass, but associations with child body composition are mixed. The purpose of this study was to examine associations between trimester-specific pregnancy PA and child body composition at 4 years. METHODS: Participants of the Minnesota Infant Nutrition, Neurodevelopment, and Obesity Study were asked to recall participation in any moderate or vigorous PA in the first (T1), second (T2) and third (T3) trimesters at about 5 years postpartum. Child fat mass and fat-free mass were measured via air displacement plethysmography at 2 weeks, 3 months and 4 years of age. Multivariate linear regression was used for analyses. RESULTS: Of 51 possible participants, 37 recalled pregnancy PA. Any vigorous PA in T3 was associated with lower child fat mass at 4 years (adjß = -1.077, p < 0.05). CONCLUSION: Late pregnancy PA may have lasting benefits for child body composition. Replication of these findings is needed in a larger sample with prospective measures.

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Several studies have suggested that maternal lifestyle during pregnancy may influence long-term health of offspring by altering the offspring epigenome. Whether maternal leisure-time physical activity (LTPA) during pregnancy might have this effect is unknown. The purpose of this study was to determine the relationship between maternal LTPA during pregnancy and offspring DNA methylation. Participants were recruited from the Archive for Research on Child Health study. At enrollment, participants' demographic information and self-reported LTPA during pregnancy were determined. High active participants (averaged 637.5 min per week of LTPA; n=14) were matched by age and race to low active participants (averaged 59.5 min per week LTPA; n=28). Blood spots were obtained at birth. Pyrosequencing was used to determine methylation levels of long interspersed nucleotide elements (LINE-1) (global methylation) and peroxisome proliferator-activated receptor-gamma (PPARγ), peroxisome proliferator-activated receptor-gamma coactivator (PGC1-α), insulin-like growth factor 2 (IGF2), pyruvate dehydrogenase kinase, isozyme 4 (PDK4) and transcription factor 7-like 2 (TCF7L2). We found no differences between offspring of high active and low active groups for LINE-1 methylation. The only differences in candidate gene methylation between groups were at two CpG sites in the P2 promoter of IGF2; the offspring of low active group had significantly higher DNA methylation (74.70±2.25% methylation for low active v. 72.83±2.85% methylation for high active; P=0.045). Our results suggest no effect of maternal LTPA on offspring global and candidate gene methylation, with the exception of IGF2. IGF2 has been previously associated with regulation of physical activity, suggesting a possible role of maternal LTPA on regulation of offspring physical activity.

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AIM: We evaluated relationships between mothers' physical activity (PA) during pregnancy and child blood pressure, aerobic fitness, and birth weight. METHODS: Anthropometrics, systolic (SBP) and diastolic (DBP) blood pressures, and aerobic fitness were measured on 20 mother/child pairs, 8-10 years postpartum. Pregnancy PA (kJ/kg.wk) was calculated from historical recall. Women were classified as meeting, or not meeting ACOG PA recommendations. RESULTS: Twelve women met ACOG recommendations, and their children had significantly lower birth weights (3.51±0.45 kg) than the more sedentary women (4.05±0.67 kg). Third trimester maternal PA was inversely related to child SBP (rs=-0.46, P=0.04) but not aerobic fitness. Birth weight was inversely related to SBP (rs=-0.75, P=0.03) if mothers did not meet PA recommendations. CONCLUSION: Results from our preliminary study suggest that maternal PA is associated with an alteration in the relationship between birth weight and SBP.

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OBJECTIVES: To investigate the effect of prenatal exposure to polychlorinated biphenyls (PCBs) and dichlorodiphenyl-dichloroethylene (DDE) on weight, height and body mass index (BMI) in adult female offspring of the Michigan fisheater cohort examined between 1973 and 1991. METHODS: 259 mothers from the Michigan fisheater cohort were studied. Prenatal exposure to PCBs and DDE was estimated by extrapolating maternal measurements to the time that the women gave birth. 213 daughters aged 20-50 years in 2000 were identified and 83% of them participated in at least one of two repeated investigations in 2001/02 (n = 151) and 2006/07 (n = 129). To assess the effect of prenatal PCB and DDE exposure on anthropometric measurements, generalised estimating equations nested for repeated measurements (2001/02 and 2006/07) and for sharing the same mother were used. We controlled for maternal height and BMI and for daughters' age, birth weight, having been breastfed and number of pregnancies. RESULTS: Maternal height and BMI were significant predictors of the daughters' height, weight and BMI. Low birth weight (<2500 g) was significantly associated with reduced adult offspring weight and BMI. The weight and BMI of adult offspring were statistically significantly associated with the extrapolated prenatal DDE levels of their mothers. Controlling for confounders and compared to maternal DDE levels of <1.503 microg/l, offspring BMI was increased by 1.65 when prenatal DDE levels were 1.503-2.9 microg/l and by 2.88 if levels were >2.9 microg/l. Prenatal PCB levels showed no effect. CONCLUSION: Prenatal exposure to the oestrogenic endocrine-disrupting chemical DDE may contribute to the obesity epidemic in women.

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Alzheimer's disease (AD) is a neurodegenerative disease characterized by dementia, senile plaques, fibrillary tangles, and a reduction of cholinergic neurons in areas of the brain, including the septal nucleus. Certain growth factors may promote the long-term survival of this subpopulation of neurons at risk. This study was undertaken to characterize growth factors' long-term effects on survival and development of neurons expressing the calcium-binding protein calbindin. In order to accomplish this, embryonic day 16 rat septal neurons were grown in bilaminar culture with astrocytes and in the absence of serum. These cultures were chronically treated with estrogen (Es), insulin-like growth factors I/II (IGF-I, IGF-II), basic fibroblast growth factor (bFGF), and nerve growth factor (NGF). Insulin-like growth factor II significantly increased the number of neurons immunoreactive for calbindin by 155%, suggesting either an increase in the survival of this subpopulation or an increase in the percentage of cells expressing calbindin. Chronic treatment with NGF, IGF-II, and Es significantly increased the number of primary neuritic processes on calbindin-positive neurons, whereas NGF and Es caused significant increases in the number of secondary processes and in the total lengths of the neuritic processes. Thus, effects of IGF-II, estrogen, and NGF on survival and maintenance of this neuronal subpopulation may be dependent on alterations in neurons which are immunopositive for calbindin.

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Cholinergic neurons of the septum are preferentially subject to degeneration in Alzheimer's disease. There is evidence that nerve growth factor, basic fibroblast growth factor, insulin-like growth factors, and estrogen all have effects on survival of this specific population of neurons at risk. We used a bilaminar culturing method to grow embryonic septal neurons from the rat in the presence of a separate glial plane but in the absence of serum. These neurons were treated with a number of factors, and neurite development of cholinergic neurons was assessed. Basic fibroblast growth factor and estrogen altered the number of primary neurites, number of secondary neurites, and mean total neurite lengths, while none of the other factors affected these end points. This would suggest a mechanism for the effects of these factors on memory.

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In this study we used differential culturing techniques to study the effects of phorbol esters on insulin receptors on neuronal and astrocytic glial cells in primary culture from the brain. 12-O-Tetradecanoyl-phorbol-13-acetate (TPA), a potent activator of protein kinase C (PKC), increased [125I]insulin binding in a time- and concentration-dependent manner with a maximally effective dose of 50 nM TPA for 2 h in glial cells. Treatment with TPA did not affect [125I]insulin binding in neuronal cells. The TPA effect on glial [125I]insulin binding was specific as evidenced by the observation that potencies of phorbol ester analogs to increase [125I]insulin binding were similar to their abilities to stimulate PKC. Competitive-inhibition experiments indicated that this effect of TPA was due primarily to an increase in the number of high affinity insulin binding sites on glial cells. Removal of the TPA after pretreatment resulted in a recovery from its effects within 6 h. The increase in glial insulin binding was not accompanied by an increase in insulin-sensitive glucose uptake, suggesting that TPA inactivates the glial cell receptors as it increases their numbers.

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Phorbol esters, potent stimulators of protein kinase C (PKC), stimulate [3H]2-deoxy-D-glucose (dGlc) uptake and [125I] insulin binding in cultured glial cells but not neuronal cells from neonatal rat brains. Using an antibody to the alpha and beta forms of PKC we have demonstrated that both neuronal and glial cells contain an immunoactive PKC of Mr approximately 80 kD, although the PKC level in neurons is greater than 4-fold that in glia. The majority of immunoactive PKC (63%) is cytosolic in glial cells although the reverse is true in neuronal cells, in which 88% of the PKC is membrane-bound in the basal state. The most potent phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), stimulates a redistribution of this enzyme in neuronal and glial cells. The TPA-stimulated translocation of PKC from cytosol to membrane precedes TPA's effects on [3H]dGlc uptake and insulin binding in glial cells.

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We have demonstrated regulation of the rat brain/Hep G2 glucose transporter gene (GT1) by Northern blot analysis with a rat brain glucose transporter cDNA probe. Incubation of both neuronal and glial cells derived from neonatal rats with 12-O-tetradecanoyl-phorbol-13-acetate induced a time- and dose-dependent increase in the steady state levels of GT1 mRNA. In glial cells, this corresponded to an increase in both the level of GT1 protein and glucose transporter activity, as demonstrated by Western blot analysis and [3H]2-deoxyglucose (dGlc) uptake studies. In contrast, in neuronal cells 12-O-tetradecanoyl-phorbol-13-acetate had no effect on either the concentration/level of the GT or [3H]dGlc uptake. These results suggest that phorbol esters regulate dGlc uptake at the transcriptional level in both neuronal and glial cells, but that the increase in expression of the GT1 gene is dissociated from posttranscriptional events involved in dGlc uptake in neuronal cells.

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We have demonstrated the expression of the rat brain/HepG2 glucose transporter gene in primary cultures of rat neuronal and glial cells by Northern blot analysis with a rat brain glucose transporter cDNA probe. Incubation of both neuronal and glial cells with insulin and insulin-like growth factor-I induced a time- and dose-dependent increase in the steady state levels of glucose transporter mRNA. The maximal response was achieved between 2-4 h and subsequently decreased. Both insulin and insulin-like growth factor-I at a dose of 1 ng/ml elicited an approximately 57% increase in glucose transporter mRNA levels in neuronal cultures after 90 min, suggesting that each peptide was acting through its own receptor. On the other hand, insulin stimulated [3H]2-deoxyglucose uptake in glial, but not neuronal, cells. These results suggest that insulin-like peptides regulate the expression of the rat brain/Hep G2 glucose transporter gene at both transcriptional and posttranscriptional levels, and that these regulatory mechanisms may be dissociated from each other. Insulin-like peptides may, therefore, participate in the control of brain energy metabolism.

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