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.

Some parameters of adipose tissue development have been studied in normal, full-term infants of gestational-diabetic mothers (GDM) and insulin-dependent diabetic mothers (IDDM). Values of skinfold thickness, body fat mass, and fat cell weight in full-term newborns of GDM and IDDM are greater than in infants of nondiabetic mothers. Fat mass enlargement in newborns of diabetic mothers seems to be caused almost exclusively by an increase in the triglyceride content of the single adipocytes. Results of determinations of fat cell weight are in fact significantly higher in newborns of GDM and IDDM and correlate closely with skinfold thickness and body fat mass: No differences resulted in the approximate estimate of fat cell number. Neither maternal weight gain during pregnancy nor pregravidic overweight seem to be directly related to the expansion of adipose tissue observed in newborns of diabetic mothers. Maternal blood glucose levels and neonatal IRI levels in cord blood significantly correlated with fat cell weight. Maternal FFA levels are not related to parameters of adipose tissue development in newborns of normal, GD, and IDD mothers. In conclusion, enlargement of body fat mass in full-term infants of GDM and IDDM is dependent on glucose availability and, thus, on the insulin-induced enhancement of triglyceride synthesis and storage in single adipocytes. Free fatty acids do not seem to play an important role in regulating the triglyceride content of fat cells in newborns of gestational-diabetic or insulin-dependent diabetic mothers.

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.

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