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.

after hydrolysis by adipose tissue lipoprotein lipase or as free fatty acids hydrolysed elsewhere. It was considered likely that both these processes were increased in large fat cells in comparison with small fat cells. It was conc1uded that the rate of uptake of exogenous ratty acids is inereased in large fat cells in comparison with small as has previously been demonstrated for triglyceride synthesis, fatty acid reesterification and lipolysis. Enlarged fat eells thus constitute a metabolie subeompartment of adipose tissue with inereased triglyceride turnover. The inereased triglyeeride turnover of enlarged fat eells is an energy wasting proeess whieh might contribut.e to regulation of fat eell size.

Rabbit alveolar saturated phosphatidylcholine (SPC) can be separated by differential and density gradient centrifugation of lung lavage into three fractions. One fraction ('B'), which is analogous to conventionally prepared alveolar surfactant, contains 46.0 +/- 5.9% (SD) of lavage SPC, and is made of large multilamellar vesicles or sheet-like structures. A second fraction ('C') does not sediment after centrifugation at 80 000 g for 90 min, contains 29.8 +/- 14.0% of lavage SPC, and a uniform population of small vesicles. This fraction incorporates 3H-palmitate administered intravenously with a small delay with respect to fraction 'B'. A third fraction ('D') contains almost all the cells of lavage and less than 5% of lavage SPC. We conclude that alveolar SPC consists of more than one compartment. The possible significance of isolated fractions is discussed.

This paper examines the removal from the airways of Curosurf, a commercial surfactant derived from porcine lungs, administered at pharmacological concentrations to newborn or adult animals. Curosurf was labelled by the addition of radioactive dipalmitoyl phosphatidylcholine (DPPC) and administered intratracheally to newborn and adult rabbits at a dose of 200 mg x kg(-1) body weight. The disappearance of DPPC from the airways and its appearance in alveolar macrophages, lung parenchyma, lamellar bodies, serum, liver, kidneys and brain was then studied for 24-48 h. The in vitro degradation of Curosurf DPPC by alveolar macrophages was also studied. During the first 3 h after instillation, large amounts of Curosurf left the airways and became associated with tissue, indicating that it mixed rapidly with the endogenous pools of surfactant. A fraction of administered DPPC became associated with the lamellar bodies, suggesting that Curosurf can be recycled. Curosurf administration did not stop the secretion of endogenous surfactant. Very little intact radioactive DPPC could be recovered at any time in alveolar macrophages, however, macrophages have the ability, in vitro, to degrade Curosurf. Newborn rabbits lose Curosurf from the lungs at a slower rate than adult rabbits. One and two days after instillation, organic extracts from the liver, kidney, brain and serum contained small but measurable amounts of radioactivity. These results indicate that Curosurf rapidly enters the pathways of surfactant metabolism and that alveolar macrophages may play an important role in the catabolism of Curosurf.

To clarify the steps following surfactant secretion, we injected adult rabbits with radioactive palmitate, lavaged the airways, removed the cells, separated by ultracentrifugation lavage components into two fractions (B and C), and followed the labeling of phospholipids of these fractions. The results were compatible with the view that total and saturated phosphatidylcholine are transferred from B to C. Furthermore, the fluxes of total and saturated phosphatidylcholine through fraction C (0.45 and 0.30 mumol . h-1 . g lung-1, respectively) were compatible with the actual estimates of surfactant recycling. The labeling of phosphatidylglycerol ruled out a simple precursor-product relationship between B and C but was compatible with a nonideal first-order relationship. The labeling of phosphatidylinositol, cardiolipin, and phosphatidylethanolamine was incompatible with the existence of a direct precursor-product relationship between B and C. The labeling of total and saturated phosphatidylcholine suggests that fraction B may be made by active surfactant, whereas fraction C may contain surfactant modified for reuptake or for reuptake and catabolism.