Conversion of palmitate to respiratory carbon dioxide by foetal tissue of man and monkey.

Abstract

ALTERATION in the amount of fat deposition in the foetus is clinically well documented for anencephalic, diabetic and low-birth weight infants1–3 and indicates that the rates of synthesis and degradation of foetal lipids, like those of the adult, are influenced by environmental and hormonal factors. It also suggests that the human foetus anabolizes or catabolizes lipids at different rates in response to pathological conditions of gestation. Observations in man and rabbit have shown that the foetus anabolizes lipids essentially from carbohydrate precursors and does not apparently catabolize lipids4,5. If this is true, fatty acids would not be catabolized to respiratory carbon dioxide (CO2) by foetal tissue in normal conditions. The assumption is open to question because slices of human foetal liver incubated with labelled fat have been shown to metabolize this substrate to respiratory carbon dioxide7.