Protein utilization, growth and survival in essential-fatty-acid-deficient rats

Abstract

AbstractThe relationship between essential fatty acids (EFA) deficiency and the utilization of dietary protein, growth rate and survival of offspring was investigated in rats during development and reproduction. EFA deficiency was induced by feeding a 200 g casein/kg-based diet containing 70 g hydrogenated coconut oil (HCO)/lkg as the only source of fat. The conversion efficiency of dietary protein was assessed as net protein utilization (NPU), using a 10 d comparative carcass technique. Consumption of the deficient diet during the 10 d assay period induced biochemical changes characteristic of mild EFA deficiency in humans (triene:tetraene 0·27 (SD 0·04) compared with 0·026 (SD 0·004) for wn-deficient controls), but there were no significant changes in growth rate or protein utilization. These variables were also unchanged when the deficient diet was fed for an additional 7 d before the assay, although triene: tetraene increased to 0.8 (SD 0·02). Feeding the deficient diet for 63 d before assay produced severe EFA deficiency (triene:tetraene 1.4 (SD 0·3) v. 0·036 (SD 0·005) for controls), a fall in growth rate (25% during assay period), and NPU (31.5 (SD 0·63) v. 39.0 (SD 0·93) for controls). These severely-EFA-deficient animals had a 30% higher fasting-resting rate of energy metabolism than that of age-matched controls. However, there was no change in the rate of endogenous N loss. Voluntary energy consumption was increased in animals fed on deficient diets, either with 200 g protein/kg, or protein free. The reduced efficiency of protein utilization could be entirely accounted for by the restricted amount of energy available for growth and protein deposition. Consumption of an EFA-deficient diet during pregnancy and lactation resulted in high mortality (11% survival rate at weaning compared with 79% for controls) and retarded growth in the preweaning offspring. It is concluded that animals are particularly sensitive to EFA deficiency during reproduction and pre- and post-natal stages of development. However, after weaning only severe EFA deficiency retarded growth, primarily through changes in energy balance.