抄録
Iodine deficiency affects all stages of life, and impaired mental function is five times as common as cretinism among populations living in iodine-deficient areas. The possibility that this could be due to an altered nutrient supply to the brain has been tested in albino rats chronically fed an iodine-deficient diet. Transport of [14C]-labelled nutrients across the blood-brain barrier (BBB) was determined in situ by the brain uptake-index (BUI) method. Feeding a low-iodine test diet (LIT) (0.0228μgI/g) to weanling Wistar/NIN rats for a short term (8 weeks) had only a modest effect on their tyroid status and no effect at all on their body or brain weight or their BBB transport of 2-deoxy-D-glucose (2-DG) as compared to control rats fed either the LIT diet+KI(-3μg I/g diet) or a locally formulated control diet of similar composition (-3μgI/g diet). On the other hand, long-term (16 weeks) dietary iodine deficiency in four different strains of rats produced a moderate hypothyroidism and significantly (p<0.05) increased transport of 2-DG across the BBB, in association with a significant decrease in their body weight but not in their brain weight. Transport of Leu, Tyr, and sucrose (the background marker) across the BBB was, however, not altered. Essentially similar observations were made in the four different strains of rats. The increased BBB transport of 2-DG in rats subjected to long-term dietary iodine deficiency probably represents an adaptive mechanism to maintain a normal glucose supply to the brain in the face of hypothyroidism.
