摘要
目的探讨生物素对2型糖尿病大鼠血糖以及糖代谢关键限速酶葡萄糖激酶(GCK)和磷酸烯醇式丙酮酸羧化酶1(PCK1)基因表达的影响。方法 90只健康Wistar大鼠根据血糖随机分为5组(正常对照组,模型组,生物素低、中、高剂量组)。正常对照组给予普通维持饲料,蒸馏水灌胃;模型组给予高脂高糖饲料,蒸馏水灌胃;生物素各剂量组给予高脂高糖饲料同时分别给予生物素0.6、3.0和6.0 mg/kg BW灌胃。在高脂高糖饲料喂养2月后,应用小剂量链脲佐菌素腹腔注射的方法建立2型糖尿病大鼠模型。于造模第10周进行OGTT实验后,处死大鼠。检测血糖、血清胰岛素、肝糖原、肌糖原等指标,用RT-PCR方法检测糖代谢关键限速酶GCK、PCK1基因的表达。结果与模型组相比,生物素各剂量组对空腹血糖、血清胰岛素没有影响,但生物素高剂量组血糖曲线下面积明显下降(P<0.05),餐后30 min血糖值也显著降低(P<0.05)。生物素中剂量组和高剂量组肌糖原含量明显下降(P<0.05)。生物素对糖代谢关键限速酶GCK、PCK1的表达有影响,分别出现了明显的基因表达上调和下调(P<0.05)。结论生物素可能通过影响糖代谢关键酶GCK和PCK1的活性,促进糖酵解和糖原合成而抑制糖异生,从而影响餐后血糖应答。
Objective To explore the effect of biotin on blood glucose regulation in rats and its possible mechanism. Methods According to initial body weight and blood glucose,we randomly divided the 90 Wistar rats into 5 groups: the normal control group,model group,biotin low-dose group( 0. 6mg / kg BW),biotin medium-dose group( 3. 0mg / kg BW) and biotin high-dose group( 6. 0 mg / kg BW). After 2 months,the rats with HFS feed were injected with STZ( 25 mg / kg BW) to manufacture diabetic rat model. After the OGTT experiment at 10 th week,the blood glucose,insulin,liver / muscle glycogen and other biochemical indexes were detected. The GCK,PCK1 mRNA expression were measured with RT-PCR method. Results Biotin has a certain improvement on postprandial glucose in diabetic rats. Compared with the model group,the AUC and the30min postprandial blood glucose of biotin high-dose group were significantly decreased( P 〈0. 05). Biotin can affect some key enzyme gene in glucose metabolism,such as GCK,PCK1. Conclusion The possible mechanism of the decreasing biotin blood sugar in diabetic rats may by promoting the synthesis of glycogenand reducing gluconeogenesis.
出处
《卫生研究》
CAS
CSCD
北大核心
2015年第2期185-189,195,共6页
Journal of Hygiene Research
基金
国家自然科学基金青年基金(No.81302428)