Effect of vitamin D Deficiency and 1,25-dihydroxyvitamin D3 on metabolism and D-glucose transport in rat cerebral cortex

We previously demonstrated that feeding rats Steenbock and Black's rickets‐inducing diet produces remarkable changes in the metabolic pattern of the in testinal mucosa, kidney, and liver and in some membrane transport Systems of intestinal mucosa and kidney. 1,25‐Dihydroxyvitamin D3 administration to rachitic rats did not always prove to be effective in restoring normal values. We have now investigated the effect of 1,25‐dihydroxyvitamin D3 on the levels of some metabolites in rat cerebral cortex, on the activity of some enzymes, and on the transport of 2‐deoxy‐D‐glucose and D‐glucose in synaptosomes. Our experiments were carried out on three rat groups: control, rachitic, and rachitic treated with 1,25‐dihydroxyvitamin D3. The decrease in phosphorus content and the increase in citrate concentration observed in rachitic rat cerebral cortex were corrected by 1,25‐dihydroxyvitamin D3 treatment. The activity of acetylcholinesterase, glucose‐6‐phosphate dehydrogenase, and acyl phosphatase significantly increased in rachitic rat synaptosomes, as well as NAD+‐dependent isocitrate dehydrogenase in cerebral cortex mitochondria; the administration of 1,25‐dihydroxyvitamin D3 to rachitic rats restored enzyme levels to normal. The transport of 2‐deoxy‐D‐glucose and D‐glucose in rachitic rat synaptosomes was lower than in the control group and returned to control values in consequence of 1,25‐dihydroxyvitamin D3 treatment. The results reported here support the hypothesis of a participation of 1,25‐dihydroxyvitamin D3 in some aspects of cerebral cortex metabolism.