Effects of prenatal alcohol exposure on uncoupling protein in brown adipose tissue in neonatal rats

Thermoregulatory deficits observed in neonatal rats exposed prenatally to alcohol may be due to peripheral and/or central dysfunction. One of the major mechanisms available to newborn mammals to generate heat is "nonshivering thermogenesis" in brown adipose tissue (BAT). In this study, the effects of prenatal alcohol exposure on the functional status of brown adipose tissue was assessed by immunoblot analysis of the content of mitochondrial uncoupling protein (UCP). BAT excised from 1- and 20-day-old male and female offspring from either alcohol-treated, pair-fed controls or standard control dams were analyzed. There were no effects of prenatal alcohol exposure on the UCP content. There was, however, a significant increase due to age. These results suggest that thermoregulatory deficits seen in alcohol-exposed offspring are not due to a deficiency in the concentration of mitochondrial UCP, and indicate a more central mechanism.