Homeostasis of circulating retinol

Circulating retinol concentrations are homeostatically
regulated to remain constant, despite great variations
in the dietary supply and liver stores of vitamin
A. The controlled release of vitamin A from liver stores
is necessary to provide tissues with optimal amounts
of retinol, without releasing excessive amounts which
would lead to toxicity. Although various schemes for
the homeostasis of circulating retinol have been proposed,
an unequivocal mechanism has not yet been
established.
The concentration of retinol bound to plasma RBP
is maintained within a normal range of concentrations,
referred to as its homeostatic set point, as long
as there is some minimal concentration of vitamin A
in the liver and in extrahepatic tissues. Thus rats fed a
vitamin A-defi cient diet maintained a relatively stable
plasma retinol level, which did not drop below 30 μg
per 100 mL until liver reserves fell below 10 μg g–1
tissue (Underwood et al., 1979). Control of plasma
retinol concentration is mediated by factors that affect
the balance between retinol input to plasma and
retinol output from plasma. Controlling factors include
the enzymes that esterify retinol and hydrolyse
retinyl esters in the tissues. The activity of hydrolytic
enzymes is enhanced during vitamin A deprivation,
releasing holoRBP into the bloodstream. The activity
of esterifying enzymes, on the other hand, is enhanced
when vitamin A intake is plentiful, allowing surplus
vitamin A to be stored. Ultimately, the set point
for plasma retinol depends on the rate of release of
holoRBP from the liver. Underwood proposed that
hepatic secretion of retinol is controlled by a signal
generated in proportion to the uptake or utilization
of retinol in extrahepatic target tissues.
The plasma retinol homeostatic set point is infl uenced
by several dietary and hormonal factors; these
include protein, calorie and zinc nutriture, and fl uctuating
steroid hormone levels that occur during the
oestrous cycle or as a result of stress. It is likely that
steroid hormones act by infl uencing the synthesis of
RBP (Borek et al., 1981). Ahluwalia et al. (1980) used
hypophysectomized rats to demonstrate that without
growth there was no vitamin A utilization. They
showed that, in addition to dietary protein, growth
hormone was required for mobilization of liver vitamin
A stores. The data suggested that growth hormone
may play an important role in vitamin A homeostasis
by regulating retinol entry at the tissue level.