Neonatal Fat Mass Research Articles

Intrafetal infusion of leptin suppresses expression of leptin mRNA and increases the proportion of multilocular adipose tissue in fetal perirenal fat in the sheep

Leptin, a 16kDa polypeptide hormone, is synthesised and secreted by adipocytes and acts to regulate energy stores and energy expenditure in the adult. In the newborn infant, there is a positive correlation between cord blood leptin concentrations and neonatal fat mass but it is unknown whether leptin can act to regulate the endocrine or metabolic characteristics of adipose tissue before birth. We have therefore tested the hypothesis that an intrafetal infusion of leptin will act to alter on leptin mRNA expression and the morphological characteristics of perirenal fat, the major fat depot in the sheep fetus during late gestation.

Effects on the foetus of exercise in pregnancy.

Maternal training during pregnancy has been the subject for numerous investigations lately, which are presented in this survey. No studies in human beings have shown any negative effect of training on the embryogenesis. During physical training a small rise in foetal heart rate of 5-25 bpm is a common finding. This could be due to a reduction in oxygen delivery or more likely stimulation from maternal vasoactive hormones or training-induced uterine contractions. Foetal growth seems to be influenced by maternal activity, as some investigations have found significantly bigger babies born by moderately trained females compared to non-trained or heavily trained women. In the latter group the reduction could be explained by a reduced neonatal fat mass. Increased maternal temperature during training has not been found to lead to any foetal abnormalities. The results indicate that moderate training during pregnancy can be recommended with observance of simple directives.

Cord Blood Leptin Reflects Fetal Fat Mass

To explore the relationship between leptin levels and fat mass at the time of birth to test the hypothesis that the level of leptin in the fetal circulation is primarily an index of fetal fat mass. Leptin concentration was measured in cord blood obtained from the offspring of 42 women. Trimmed, drained placental weight and neonatal morphometrics were obtained after delivery. The ranges in maternal weight (46.7-93.2 kg), weight gain (3.2-22.6 kg), percent body fat (10-34%), placental weight (290-688 g), birth weight (2.63-4.32 kg), neonatal fat mass (179-782 g), and cord blood leptin (1.7-26.7 ng/mL) were wide. The only morphometric variable that explained a significant portion of the variation in cord blood leptin levels was neonatal fat mass (r2 = 0.41), and this relationship was not significantly improved by best subset regression of additional fetal and placental morphometric variables (r2 = 0.46). These data support the hypothesis and suggest that in the fetus, as in the child and the adult, fat mass is the major determinant of circulating leptin levels.

Anthropometric estimation of neonatal body composition

OBJECTIVE: Estimation of neonatal body composition can be useful in the understanding of fetal growth. However, body composition methods such as total body water and total body electric conductivity are expensive and not readily available. Our primary purpose was to develop an anthropometric model to estimate neonatal body composition and prospectively validate the model against total body electric conductivity and secondarily tocompare our anthropometric model and a previously published anthropometric formula with total body electric conductivity. STUDY DESIGN: A total of 194 neonates had estimates of body composition according to total body electric conductivity (group 1). Parental morphometrics, gestational age, race, sex, parity, and neonatal measurements including birth weight, length, head circumference, and skinfolds (triceps, subscapular, flank, and thigh) were correlated with body fat by use of stepwise regression analysis. The model was validated in a second group of 65 neonates (group 2). RESULTS: There were no significant differences in any of the parental or neonatal measurements between groups 1 and 2. In group 1, 78% of the variance in body fat with the use of total body electric conductivity was explained by birth weight, length, and flank skifold ( R 2 = 0.78, p = 0.0001). When prospectively validated by the subjects in group 2, the model had significant and stronger correlation ( R 2 = 0.84, p = 0.0001) with body fat estimated by total body electric conductivity as compared with the other anthropometric model ( R 2 = 0.54, p = 0.0001). There was no significant ( p = 0.11) difference between our anthropometric estimate of body fat and total body electric conductivity. CONCLUSIONS: The anthropometric model developed can be used to reasonably predict neonatal body fat mass at birth.

Maternal carbohydrate metabolism and its relationship fetal growth and body composition

OBJECTIVE: Our purpose was to correlate maternal carbohydrate metabolism and parental morphometric measurements with neonatal birth weight, body composition, and placental weight. STUDY DESIGN: Sixteen singleton (six control and 10 abnormal glucose tolerance) infants had placental weight, birth weight, and estimates of body composition performed within 24 hours of birth. Independent variables considered were (1) maternal and paternal demographic and morphometric measures, (2) neonatal sex and gestational age, and (3) estimates of maternal carbohydrate metabolism, including basal hepatic glucose production, insulin response, and insulin sensitivity. All metabolic measurements were performed before conception and in early (12 to 14 weeks) and late (34 to 35 weeks) gestation. Best-fit stepwise regression analysis was used to relate the independent variables with placental weight, neonatal birth weight, fat-free mass, and fat mass. RESULTS: Insulin sensitivity in late gestation had the strongest correlation with placental weight ( R 2 = 0.28), neonatal birth weight ( R 2 = 0.28), and fat-free mass ( R 2 = 0.33). In contrast, insulin sensitivity before conception had the best correlation with neonatal fat mass ( R 2 = 0.15). Including all significant independent variables in the model improved the correlations for placental weight ( R 2 = 0.58), birth weight ( R 2 = 0.48) fat-free mass ( R 2 = 0.53), and fat mass ( R 2 = 0.46). CONCLUSION: Maternal insulin sensitivity had stronger correlations with fetoplacental growth in comparison with maternal demographic or mophometric factors.

Neonatal morphometrics after endurance exercise during pregnancy

This study was designed to test the hypothesis that continuation of a regular running and/or aerobics program during late pregnancy at or above 50% of preconceptional levels limits fetal growth. Accordingly, detailed neonatal morphometric data were gathered in the offspring of two groups: 77 well-conditioned recreational runners and aerobic dancers who were delivered at term after continuing their exercise regimen at or above 50% of the preconceptional level throughout pregnancy and 55 matched controls. Daily exercise performance was quantitated before conception and throughout pregnancy. Significant reductions in birth weight (-310 gm), birth weight percentile (-20), ponderal index (-0.24), its percentile (-30), and the fetoplacental weight ratio (-0.7) were seen in the offspring of the exercise group whereas crown-heel length (51.4 cm) and head circumference (35.0) were similar in the two groups. Reductions in two-site skin-fold thickness (-1.5 mm), skin-fold percentile (-30), calculated percent body fat (-5.0%), and fat mass (-220 gm) in the offspring of the exercise group confirmed the asymmetric pattern of growth restriction and indicated that approximately 70% of the difference in birth weight could be explained by the difference in neonatal fat mass. In runners, the relative level of exercise performance in the last 5 months of pregnancy explained 40% of the variability in birth weight over an 1100 gm birth weight range. We conclude that continuation of a regular aerobic or running program at or above a minimal training level during late pregnancy results in an asymmetric pattern of growth restriction that primarily impacts on neonatal fat mass.

Ultrasonographic Estimation of Fetal Body Composition for Children of Diabetic Mothers

The authors hypothesized that ultrasound-generated measurements of the fetus could be used to predict body composition for children of diabetic mothers. Seven ultrasonically identifiable fetal morphometric parameters were measured on 21 fetuses of diabetic mothers within 7 days of delivery. These seven individual measurements were then matched to neonatal morphometric estimations of body composition by means of stepwise regression analysis. Ultrasound variables which were found to show significant correlation to the newborn estimates of body composition were combined to generate an equation that could predict neonatal lean body mass and fat mass. Neonatal lean body mass could be predicted with R = .93 (P less than .001, 95% confidence limits .80-.98). Neonatal fat mass could be predicted with R = .81 (P less than .001, 95% confidence limits .55-.92). Prospective evaluation of the regression equations in an additional 18 patients showed no significant difference between ultrasound-predicted body composition and newborn morphometric estimation of body composition. The authors conclude that estimations of fetal body composition are possible, and may provide a valuable tool in the identification of fetal growth abnormalities.

Neonatal morphometrics after endurance exercise during pregnancy

This study was designed to test the hypothesis that continuation of a regular running and/or aerobics program during late pregnancy at or above 50% of preconceptional levels limits fetal growth. Accordingly, detailed neonatal morphometric data were gathered in the offspring of two groups: 77 well-conditioned recreational runners and aerobic dancers who were delivered at term after continuing their exercise regimen at or above 50% of the preconceptional level throughout pregnancy and 55 matched controls. Daily exercise performance was quantitated before conception and throughout pregnancy. Significant reductions in birth weight (-310 gm), birth weight percentile (-20), ponderal index (-0.24), its percentile (-30), and the fetoplacental weight ratio (-0.7) were seen in the offspring of the exercise group whereas crown-heel length (51.4 cm) and head circumference (35.0) were similar in the two groups. Reductions in two-site skin-fold thickness (-1.5 mm), skin-fold percentile (-30), calculated percent body fat (-5.0%), and fat mass (-220 gm) in the offspring of the exercise group confirmed the asymmetric pattern of growth restriction and indicated that approximately 70% of the difference in birth weight could be explained by the difference in neonatal fat mass. In runners, the relative level of exercise performance in the last 5 months of pregnancy explained 40% of the variability in birth weight over an 1100 gm birth weight range. We conclude that continuation of a regular aerobic or running program at or above a minimal training level during late pregnancy results in an asymmetric pattern of growth restriction that primarily impacts on neonatal fat mass.

Adipose tissue development "in utero". Relationships between some nutritional and hormonal factors and body fat mass enlargement in newborns.

Some metabolic and hormonal variables, thought to affect adipose tissue development “in utero” were studied in a group of 50 presumably healthy mothers and in their full-term infants. No sex-related differences were observed at birth in skinfold thickness, body fat mass, fat cell volume or fat cell number. Body fat mass in newborns was significantly correlated to fat cell size (r=0.75; p< 0.001), but not to fat cell number. Weight gain during pregnancy but not prepregnancy weight was correlated to fat cell volume in the newborn (r=0.67; p<0.001) and to body fat mass (r=0.66; p< 0.001). Maternal placental lactogen levels correlated to decreased glucose tolerance in the mothers (r= 0.62; p<0.001), as well as to body fat mass (r= 0.61; p<0.001) and fat cell size (r=0.58; p< 0.001) in newborns. Neonatal plasma insulin levels in addition correlated with body fat mass (r=0.39; p< 0.05) and fat cell weight (r=0.69; p<0.001) of the neonate. Placental NEFA transfer could be demonstrated, but there was no correlation between maternal plasma NEFA levels and neonatal body fat mass or fat cell weight. Similarly, maternal insulin and growth hormone levels were not correlated with neonatal body fat mass or with fat cell size or number. Thus the nutritional and hormonal factors considered do not appear to be involved in fat cell multiplication. During intrauterine life, in full-term infants of presumably healthy mothers, fat mass expansion seems to occur almost exclusively by means of fat cell hypertrophy.