The development of beta 1-adrenoceptors in brown adipose tissue following prenatal alcohol exposure.

Prenatal alcohol exposure delays the development of thermoregulation in newborn rats. Newborns generate heat by the sympathetic nervous system's activation of nonshivering thermogenesis in brown adipose tissue (BAT). In this study, the effects of prenatal alcohol exposure on the development of the beta-adrenergic receptor system of BAT was investigated by assessing the number and pharmacological properties of beta-adrenergic receptors in BAT in 1-, 5-, 10-, and 20-day-old offspring. Pregnant dams were given either a liquid diet with 35% of the calories derived from alcohol, a liquid diet without alcohol for any effects of the liquid diet administration, or ad lib food and water. Offspring from the alcohol prenatal treatment group had a greater number of beta 1 adrenergic receptors compared to offspring from both from the pair-fed and lab chow control groups, which did not differ from each other. The greater number of receptor sites in 5-day-old subjects suggests that the number of binding sites in alcohol-exposed BAT cells continues to rise due to the absence of sufficient neurotransmitter, and perhaps reflects a delay in the arrival of sympathetic nervous system neurons. During the second and third postnatal weeks, when NE concentrations are rising and reaching asymptotic levels, the number of beta 1 adrenergic receptors in BAT of control subjects is decreasing. This expected compensatory "downregulation" response in receptor concentration was not seen in BAT from subjects exposed to alcohol prenatally. These findings may have important implications for understanding the effects of prenatal alcohol exposure on developing plasticity in the peripheral nervous system.