Alterations in fetal adipose tissue leptin expression correlate with the development of adipose tissue

Control pig fetuses and fetuses hypophysectomized (hypox) at 70 days of gestation were treated with hormones on day 90. At 105 days of gestation, subcutaneous adipose tissue was prepared for morphological studies, leptin Northern blot and Western blot analysis. Fetal ontogeny studies showed that leptin mRNA in adipose tissue increased with morphological development, and the highest level of leptin mRNA was observed in 105-day fetal pigs. In hyper fetuses, levels of leptin mRNA were similar to those in controls. Treatment with either hydrocortisone (HC) or thyroxine (T-4) resulted in a slight increase in leptin mRNA levels in hyper fetuses but not in intact fetuses. Supplementation with both HC and T-4 markedly stimulated leptin mRNA expression in both hyper and intact fetuses. Morphological data showed that hyper slightly enhanced lipid accretion and treatment of hyper fetuses with HC and T-4 increased lipid accretion to a greater degree than did either HC or T-4 alone. However, serum leptin levels were not influenced by age, hyper or hormone treatment. Leptin protein expression was not detected in adipose tissue of hyper or intact fetuses regardless of hormone treatment. Leptin protein was detected in adipose tissue of 7-day-old pigs and placenta. As compared to 7-day postnatal adipose tissue, placenta showed a higher level of leptin protein expression. Leptin mRNA expression in feta I adipose tissue was not correlated with body weight and organ weight. The expression of long-form leptin receptor mRNA was detected in fetal adipose tissue. Our results indicate that adipose tissue leptin may not be the main source of serum leptin in the fetus and may not be involved in general prenatal growth and development. But adi pose tissue leptin may act as an autocrine or paracrine factor in the development of fetal adipose tissue. Copyright (C) 2000 S. Karger AG, Basel.