Zhang H, Osada K, Sone H, Furukawa Y
Department of Applied Biological Chemistry, Faculty of Agriculture, Tohoku University, Sendai Japan.
J Nutr Sci Vitaminol (Tokyo). 1997 Jun;43(3):271-80. doi: 10.3177/jnsv.43.271.
The effect of biotin administration on the glucose tolerance of streptozotocin (STZ)-induced diabetic Wistar rats was investigated. STZ-induced diabetes was induced by intraperitoneal injection of streptozotocin (45 mg/kg body weight as a single dose). The impaired glucose tolerance in response to an oral glucose load (1.8g per kg body weight) in STZ-induced diabetic rats (STZ-rat) was partially improved by intraperitoneal administration of biotin for 15 days (100 micrograms/rat/day). However, a recovery in the STZ-rat's insulin secretion was not found after biotin administration. To help clarify the mechanism underlying the improvement in glucose tolerance seen with biotin treatment, glucokinase and hexokinase activities were determined in the liver and pancreas. In STZ-rats that had received biotin (STZ-biotin rats), glucokinase activity was higher by 3.4-fold in liver and by 2.4-fold in pancreas than in the STZ-rats. The biotin level of STZ-rats was significantly lower in the liver and pancreas than that of the control rats (no STZ administration); but in STZ-biotin rats, the level in these organs recovered to the control level. These results demonstrate that injected biotin can improve glucose handling without increasing insulin secretion in STZ-rats.
研究了生物素给药对链脲佐菌素（STZ）诱导的糖尿病Wistar大鼠葡萄糖耐量的影响。通过腹腔注射链脲佐菌素（45mg/kg体重，单剂量）诱导STZ诱导的糖尿病。对STZ诱导的糖尿病大鼠（STZ大鼠）口服葡萄糖负荷（1.8g/kg体重）时受损的葡萄糖耐量，通过连续15天腹腔注射生物素（100μg/大鼠/天）得到部分改善。然而，生物素给药后未发现STZ大鼠的胰岛素分泌恢复。为了帮助阐明生物素治疗改善葡萄糖耐量的潜在机制，测定了肝脏和胰腺中的葡萄糖激酶和己糖激酶活性。在接受生物素的STZ大鼠（STZ-生物素大鼠）中，肝脏中的葡萄糖激酶活性比STZ大鼠高3.4倍，胰腺中高2.4倍。STZ大鼠肝脏和胰腺中的生物素水平显著低于对照大鼠（未注射STZ）；但在STZ-生物素大鼠中，这些器官中的生物素水平恢复到对照水平。这些结果表明，注射生物素可改善STZ大鼠的葡萄糖处理能力，而不增加胰岛素分泌。
