Thermogenesis secondary to transdermal water loss causes growth retardation in essential fatty acid-deficient rats

Abstract

Manifestations of essential fatty acid (EFA) deficiency in rats include growth retardation and increased transdermal water loss. The extra metabolic energy requirement could be caused by greater evaporative water loss from the skin surface. To test this hypothesis, 38 weanling rats were randomly assigned to one of two environments, control (CE) at 20°C and 40% humidity or warm/humid (WHE) at 30°C and 90% humidity. Half of the 20 CE rats were fed an EFA-adequate diet and the other 10 an EFA-deficient diet; the 18 WHE rats were also equally partitioned to the two diets. CE and WHE animals were independently group-fed to maintain equal energy intakes within each environment. Weight gain at 90 days was lower for CE EFA-deficient rats than for CE EFA-adequate rats ( P < .0001). Growth rates in the WHE to 140 days did not difer. Mean weights at 90 days were as follows: CE EFA-adequate, 196 g; CE EFA-deficient, 148 g; WHE EFA-adequate, 148 g; WHE EFA-deficient, 135 g. In both CE and WHE animals, the triene/tetraene ratio of both serum and liver phospholipids (PL) was 100-fold greater for EFA-deficient versus EFA-adequate diets. PL fatty acids of liver in CE and WHE EFA-deficient rats contained 2.09 and 1.92 μg of 20:3ω9 per μg phosphorus (P i), respectively, compared with 0.03 and 0.02 μg 20:3ω9/μg P i in CE and WHE EFA-adequate rats. These results indicate equivalent degrees of EFA deficiency in the two environments. From the lack of growth retardation of EFA-deficient animals in the WHE compared with CE, we conclude that growth stunting caused by EFA deficiency is predominantly due to the increase in thermogenesis required to counter heat loss from accelerated transdermal water evaporation.