Matsuo T, Shimakawa K, Suzuoki Z
J Nutr. 1983 Sep;113(9):1784-90. doi: 10.1093/jn/113.9.1784.
Male weanling rats, fed a riboflavin-deficient diet for 14 days showed impairments in reactivity to the hyperphagic action of either insulin or 2-deoxy-D-glucose (2DG) and in sensitivity to the diabetogenic action of streptozotocin or alloxan. The intraperitoneal injection of riboflavin (160 micrograms/rat) resulted in an immediate restoration in FAD-dependent activation of erythrocyte glutathione reductase and in the reactivity of food intake to insulin, whereas the reactivity of food intake to 2DG was restored after 3 days of riboflavin repletion. The sensitivity to diabetogenic agents was not restored solely by the riboflavin injection but required 3 hours of feeding as well. These findings indicate that the riboflavin deficiency caused some defects at specific glucosensitive sites localized in the pancreas and the brain and that some metabolic processes were necessary to restore the sensitivity.
雄性断乳大鼠喂食缺乏核黄素的饲料14天后，对胰岛素或2-脱氧-D-葡萄糖（2DG）的促食作用的反应性以及对链脲佐菌素或四氧嘧啶致糖尿病作用的敏感性出现损伤。腹腔注射核黄素（160微克/只大鼠）可使红细胞谷胱甘肽还原酶的FAD依赖性激活以及食物摄入量对胰岛素的反应性立即恢复，而食物摄入量对2DG的反应性在核黄素补充3天后恢复。对致糖尿病药物的敏感性并非仅通过注射核黄素就能恢复，还需要3小时的喂食。这些发现表明，核黄素缺乏在胰腺和大脑中的特定葡萄糖敏感位点造成了一些缺陷，并且一些代谢过程对于恢复敏感性是必要的。
