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Biology Laboratories, Central Research Division, Takeda Chemical Industries, Ltd., Jusohonmachi, Yodogawa-ku, Osaka 532, Japan
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 µg/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.
KEY WORDS: riboflavin deficiency glucosensitive site diabetogenic agent
Manuscript received 11 March 1983.