Epidemiological evidence shows that small size at birth is associated with an increased risk of developing cardiovascular and metabolic disease in adult life. We have examined the relationships between size at birth and maternal body composition and protein turnover in normal pregnant women. A group of 27 multiparous Caucasian women with singleton pregnancies were studied at around 18 and 28 weeks' gestation. Body composition was determined by anthropometry, and whole-body protein turnover was estimated by using a single oral dose of [15N]glycine and the end-product method. The baby's weight and length were measured within 48 h of birth. Mothers with a greater lean body mass had higher rates of protein turnover at 18 weeks' gestation. This association was largely accounted for by differences in the mother's visceral, rather than muscle, mass. Mothers who had higher protein turnover at 18 weeks' gestation had babies that were longer at birth. After adjustment for the duration of gestation and the baby's sex, 26% of the variation in length at birth was accounted for by maternal protein synthesis at 18 weeks' gestation. Maternal protein intake was not associated with the baby's birth length. Thus the mother's ability to nourish her fetus is influenced by her body composition and her rate of protein turnover. Dietary intake does not adequately characterize this ability.
ABSTRACT. Low values of serum proteins and loss of lean body mass are commonly found in patients with chronic renal insufficiency (CRI) and especially in dialysis patients. These abnormalities have been attributed to malnutrition (i.e., an inadequate diet), but available evidence indicates that this is not the principal cause. In contrast, there is persuasive evidence that secondary factors associated with the CRI condition cause abnormalities in protein turnover and ultimately result in low serum protein levels and loss of lean body mass. Recent reports have identified some factors that could interfere with the control of protein turnover in CRI patients, including acidosis, inflammation, and/or resistance to anabolic hormones. Each of these stimulates protein breakdown in muscle and activates a common proteolytic pathway, the ubiquitin-proteasome pathway. Moreover, acidosis or inflammation suppress hepatic albumin synthesis. Understanding the biochemical mechanisms that regulate the ubiquitin-proteasome and other catabolic pathways are required to identify new strategies for preventing protein deficits that are associated with CRI.
The Relationship of Total Exchangeable Potassium and Chloride to Lean Body Mass, Red Cell Mass and Creatinine Excretion in Man