Vitamin A regulates many essential mammalian biological processes, including embryonic development. β-carotene is the main source of vitamin A in the human diet. Once ingested, it is packaged into lipoproteins, predominantly low-density lipoproteins (LDL), and transported to different sites within the body, including the liver and developing tissues, where it can either be stored or metabolized to retinoids (vitamin A and its derivatives). The molecular mechanisms of β-carotene uptake by the liver or developing tissues remain elusive. Here, we investigated the role of the LDL receptor (LDLr) in β-carotene uptake by maternal liver, placenta and embryo. We administered a single dose of β-carotene to Ldlr+/- and Ldlr-/- pregnant mice via intraperitoneal injection at mid-gestation and monitored the changes in β-carotene content among maternal lipoproteins and the liver, as well as the accumulation of β-carotene in the placental-fetal unit. We showed an abnormal β-carotene distribution among serum lipoproteins and reduced hepatic β-carotene uptake in Ldlr-/- dams. These data strongly imply that LDLr significantly contributes to β-carotene uptake in the adult mouse liver. In contrast, LDLr does not seem to mediate acquisition of β-carotene by the placental-fetal unit.
Keywords: LDL receptor; maternal liver; vitamin A; β-carotene uptake.