Fat Mass Expansion Research Articles

Postnatal development of adipose tissue in normal children on strictly controlled calorie intake

The relations between adipose tissue development at birth, later expansion of fat mass and the behavior of fat mass and fat cell growth from birth to 12 mo of age have been studied in normal children born to normal, obese or diabetic mothers and maintained on strictly controlled calorie intake. A simple method for fat cell size determination on microsamples of fat tissue, specifically designed for small children, is reported. In the first 3 mo of life, a marked increase of fatty tissue from 13.4 ± 0.4 to 20.3 ± 0.8 percent of total body mass was observed. Subsequently, a sharp decrease in the relative amount of fat mass occurs, probably related to an increased energy expenditure or to a slightly higher protein content in the diet. No sex related differences in body weight, body fat mass, sum of skinfold thickness or fat cell weight were found throughout the study. No significant differences in body fat mass, sum of skinfold thickness and body fat mass as percent of body weight was observed at birth and at 3 or 6 mo of age in children of obese or gestational diabetic mothers, in comparison with children of normal mothers, and no significant correlation was found between maternal adiposity (sum of skinfold thickness or pre-gravidic overweight) or glucose tolerance (blood glucose area after OGTT) and adipose tissue development in the first 6 mo of life. Thus, in children on strictly controlled intake, obesity or diabetes in the mother do not relate to the rate of fat accumulation. Moreover, no relations were found between adipose tissue development at birth and subsequent rate of fat enlargement in the first year of life. Thus, when the interference of a different calorie intake is excluded, adiposity at birth has no predictive value for possible fatness later in infancy.

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.

Importance of fixed sections in the study of adipose tissue cellularity.

IN the study of obesity in human subjects and animal models attention has recently been directed to the size and number of cells in adipose tissue. Measurements of fat cell sizes have led to the classification of hypertrophic, hyperplastic or mixed forms of obesity in animals1 and man2. A study of the literature concerning animals, however, reveals wide discrepancies in reports of the degree of hypertrophy or hyperplasia contributing to the expansion of fat mass observed in genetically3,4 or experimentally obese animals1,5–10. These discrepancies have arisen not only because different species and strains of animals were used and different fat depots were sampled, but also because different methods were used to determine fat cell size and number.