Role of noradrenergic innervation of brown adipose tissue in thermoregulatory deficits following prenatal alcohol exposure.

The development of thermoregulation in newborns is delayed by prenatal alcohol exposure in an animal model of moderate maternal drinking. Newborn mammals generate heat primarily via nonshivering thermogenesis in brown adipose tissue (BAT), which is activated by the sympathetic nervous system. In this study, the effects of prenatal alcohol exposure on the development of the sympathetic innervation of BAT was investigated by assessing the concentration of norepinephrine (NE) in interscapular BAT. Pregnant dams were given either a liquid diet with 35% of the calories derived from alcohol, a liquid diet without alcohol to control for any effects of the liquid diet administration, or ad libitum food and water. Interscapular brown adipose tissue was excised from 5-, 10-, and 20-day-old male and female offspring. At 5 days of age, alcohol-exposed pups had significantly lower NE concentrations than did pups in either control group. However, 20-day-old alcohol-exposed pups had significantly higher NE concentrations than either control group. These results suggest a delay in the development of the sympathetic activation of BAT thermogenesis, followed by a compensatory overactivation. These findings may have important implications for understanding the mechanisms underlying thermoregulatory deficits seen after prenatal alcohol exposure. In addition, these results suggest that maternal alcohol consumption may increase the risk of sudden infant death syndrome, which has been linked to inappropriate BAT thermogenesis.