Recent studies have shown that plasma concentrations of vitamin A (ret
inol) and its carrier proteins, retinol-binding protein (REP), and tra
nsthyretin (TTR), are decreased in human subjects with insulin-depende
nt (IDDM) but not with noninsulin dependent diabetes mellitus (NIDDM).
Rats made diabetic with streptozotocin (STZ) have also been shown to
have reduced levels of plasma vitamin A while its hepatic concentratio
ns elevate. The circulatory vitamin A levels remained low while its he
patic concentrations were further elevated following supplementation o
f the vitamin. The reduced circulatory status of vitamin A in diabetic
animals was not caused by its impaired intestinal absorption. Further
experimental studies have pointed to the fact that IDDM is associated
with a deficiency of vitamin A, which is secondary to an impaired tra
nsport mechanism of this vitamin from its hepatic storage to the targe
t site, such as retina of the eyes. The diabetes-associated changes in
vitamin A metabolism were reversed to normal by insulin treatment. Th
e underlying cause for decreased metabolic availability in uncontrolle
d diabetes, is not clearly understood. It appears that the increased h
epatic store of vitamin A is attributed to a decreased availability of
its carrier proteins. Subnormal vitamin A status in poorly controlled
diabetic subjects may not respond to vitamin A supplementation, rathe
r it may increase its load in the liver lending to hepatoxicity. These
results clearly suggest that there is a need for further research ide
ntifying the importance of vitamin A in diabetes mellitus. (C) Elsevie
r Science Inc. 1997.