Abstract
Hepatic β-adrenergic receptors (β-ARs) play a pivotal role in mobilization of reserves via gluconeogenesis and glycogenolysis to supply the animal with its energy needs during decreased nutrient availability. Using a unique nutrient-deprived baboon model, we have demonstrated for the first time that immunoreactive hepatic β(1)- and β(2)-AR subtypes are regionally distributed and localized on cells around the central lobular vein in 0.5 and 0.9 gestation (G) fetuses of ad libitum fed control (CTR) and maternal nutrient restricted (MNR) mothers. Furthermore, MNR decreased fetal liver immunoreactive β(1)-AR and increased immunoreactive β(2)-AR at 0.5G. However, at 0.9G, immunohistochemistry and Western blot analysis revealed a decrease in β(1)-AR and no change in β(2)-AR levels. Thus, MNR in a nonhuman primate species has effects on hepatic β(1)- and β(2)-ARs that are receptor- and gestation stage-specific and may represent compensatory systems whose effects would increase glucose availability in the presence of nutrient deprivation.