Endocrine Abstracts

Leptin, the 16 kDa product of the obese gene, and uncoupling proteins (UCP) are both involved in energy expenditure. Piglets have recently been shown to express UCP2, it has been speculated that the induction of UCP2 in adipose tissue by leptin may stimulate thermogenesis. The aim of this study was to investigate the effect of leptin administration on body temperature, leptin and UCP2 mRNA. Ten Meishan sows gave birth naturally at term and siblings were paired by birth weight and gender. On day 3 of life, piglets were randomly allocated to either leptin (L: n=6) or placebo (P: n=6) group and were subsequently administered intravenously with either leptin (1ml/kg: conc. 50ng/ml) or a saline placebo (1ml/kg) at 10.00 hrs daily for 6 days. Rectal temperature was measured just prior to treatment. On day 9 of life, the animals were humanely euthanased to enable tissue sampling. Total RNA was isolated from the adipose tissue mRNA abundance was examined by RT-PCR. Results are expressed in arbitrary units as a percentage of an 18S rRNA internal control. Plasma concentrations of leptin were determined by RIA, General Linear Model ANOVA was used to assess differences between each treatment groups. At the start of the study rectal temperature (38.1±0.4 degrees C: mean±SEM) and plasma leptin concentrations (2.53±0.05 ng/ml) were similar. On day 9 body temperature was lower (P<0.05) in piglets that received leptin (38.6±0.2; L: 39.0±0.1 degrees C) and plasma leptin was higher (P<0.05) in the leptin group (L:2.77±0.11; P:2.59±0.04 ng/ml). Daily leptin administration did not influence the abundance of leptin (L:1155±285; P:1004±214 arbitrary units) or UCP2 (L:11.22±2.77; P:10.50±2.73 arbitrary units) mRNA. In conclusion, the chronic administration of recombinant (human) leptin influenced the thermoregulatory ability of the newborn pig without concomitant changes in UCP2 or leptin abundance.