Intrauterine growth and adipose tissue development

Abstract

Body fat mass (BFM), skinfold thickness (ST), and fat cell weight (FCW) have been studied in 86 newborn infants with different maturity and different intrauterine growth, and in parabiotic twins. Preterm infants (35.5 +/- 0.4 wk) with body weight appropriate for gestational age had lower values of BFM and sum of ST as compared to the control group, without differences in FCW (0.23 +/- 0.03 versus 0.22 +/- 0.02 micrograms). In infants born between 30 and 41 wk of gestation with body weights at birth appropriate for gestational age, ST and BFM progressively increase with gestational age, while the FCW remains constant. These observations suggest that fat mass growth in the last 2 months of fetal life, essentially depends on fat cell replication. In full-term large-for-date babies, bFM resulted significantly greater than in controls both in absolute values (p less than 0.001) and in percentage values of total body weight (p less than 0.001). The FCW in large for date newborns resulted significantly greater than in controls (0.50 +/- 0.06 versus 0.22 +/- 0.2 micrograms, p less than 0.001). In full-term small-for-date newborns BFM, ST, and FCW resulted significantly lower than in controls (p less than 0.001). In full-term newborns with different body weight at birth, fat cell weight was correlated to BFM (r = 0.67; p less than 0.01), to BFM as percentage of body weight (r = 0.67; p less than 0.001) and to ST (r = 0.73; p less than 0.001). In three couples of identical parabiotic twins, the larger baby of every pair showed even greater values of BFM, ST, and FCW and fat cell weight than the respective sibling. These observations suggest that in newborns with different intrauterine growth, a different triglyceride content in single adipocytes largely explains the variations in fat mass development.

Association of adiponectin polymorphism with cord blood adiponectin concentrations and intrauterine growth

“…1,30,31 This positive relationship between the two parameters in newborns may be explained by a lack of negative feedback on adiponectin production because of few hypertrophic adipocytes, an increased amount of fat mass together with an increased number of small adipocytes, low percentage of body fat with a different fat distribution and relatively abundant brown adipose tissue secreting adiponectin. 8,32,33 In the study of ADIPOQ SNPs and cord blood adiponectin concentrations, Rothenbacher et al 22 investigated associations of ADIPOQ SNPs (rs17300539, rs266729 and rs1501299) with cord blood adiponectin concentrations in neonates, most of whom were of German ethnicity, and showed that the subjects with rs266729 CG or GG genotype had higher cord blood concentrations of adiponectin than those with the CC genotype after adjustment for gender and gestational age; these findings were consistent with the present study. However, the relationship between the ADIPOQ SNPs and birth weight was not presented in the German study.…”

“…First, in the second half of intrauterine life, fetal adipose tissue rapidly expands with increasing size and number of adipocytes, and is mainly composed of small newly differentiated adipocytes, which secrete more adiponectin to increase adipocyte proliferation and lipid accumulation. 33,38 Additionally, a negative feedback on adiponectin production caused by fat mass with hypertrophic adipocytes has not been found in newborns. Although further investigations are needed, the genetic effects of rs266729 SNP on adiponectin promoter activity is likely to alter adipose tissue metabolism in intrauterine life, unlike in adults.…”

Independent effects of weight gain and fetal programming on metabolic complications in adults born small for gestational age

“…The mismatch between a poor intrauterine environment and more favourable postnatal conditions could result in abnormal body composition, which in turn will promote IR. Individuals born SGA suffer from a severe reduction of fat mass at birth [8,9], but a large proportion of them will experience a rapid postnatal catch-up in growth during the first year of life [10,11]. The association between metabolic disorders and low BW appears stronger when small size at birth is followed by early catch-up growth [7,12,13].…”

Time Course of Catch-up in Adiposity Influences Adult Anthropometry in Individuals Who Were Born Small for Gestational Age

“…However, this complex phenomenon is associated with substantial change in body distribution. Individuals who were born SGA display a peculiar growth pattern of adiposity: severely reduced at birth (3,4), adiposity dramatically increases during the catch-up growth period in children who were born SGA, as evidenced by the noticeably increased body mass index (BMI) during infancy (5,6). Furthermore, it has been shown that children who were born SGA and displayed catch-up growth during infancy showed an increased body fat mass with a more central fat distribution in comparison with children who were born with normal birth size (6).…”