Objective:Because children with congenital hyperinsulinism(HI) caused by recessive loss of function mutations in the adenosine triphosphate (ATP)-dependent potassium channel(KATP-HI) are not leucine sensitive,we evalu...Objective:Because children with congenital hyperinsulinism(HI) caused by recessive loss of function mutations in the adenosine triphosphate (ATP)-dependent potassium channel(KATP-HI) are not leucine sensitive,we evaluated for protein induced hypoglycemia with oral protein tolerance tests. Study design:Blood glucose and insulin concentrations were measure devery 15 minutes for 3 hours after an oral protein loadin children with KATP-HI (n=11) and compared with those of children with glutamate dehydrogenase HI (n=12) and control subjects (n=12). Results:Similar to children with glutamate dehydrogenase HI,patients with KATP-HI displayed protein-induced hypoglycemia (10/11)with blood glucose concentrations declining by 17 to 69 mg/dL. In contrast,oral proteinhad little effect on blood glucose concentrations in control subjects.Conclusions:Protein induced hypoglycemia is a feature of KATP-HI,despite the absence of leucine sensitivity. The results indicate that amino acids can stimulate insulin secretionvia a glutamate dehydrogenase and KATP channel-independent pathway.展开更多
目的探讨内脂素基因过表达对高脂诱导胰岛素抵抗（IR）大鼠胰岛素敏感性的影响。方法构建大鼠内脂素基因真核表达质粒，并用该质粒转染高脂喂养诱导的IR大鼠模型。在转染前后采用两次高胰岛素-正糖钳夹技术评价大鼠胰岛素敏感性的变化...目的探讨内脂素基因过表达对高脂诱导胰岛素抵抗（IR）大鼠胰岛素敏感性的影响。方法构建大鼠内脂素基因真核表达质粒，并用该质粒转染高脂喂养诱导的IR大鼠模型。在转染前后采用两次高胰岛素-正糖钳夹技术评价大鼠胰岛素敏感性的变化。结果成功构建了内脂素真核表达载体pcDNA3．1内脂素。实验组大鼠在pcDNA3．1内脂素质粒注射后3d血浆内脂素水平较注射前明显升高（2．19±0．36 vs 0．98±0．27，P〈0．01）；在两次胰岛素钳夹中，pcDNA3．1内脂素质粒注射后葡萄糖输注率较注射前明显升高[（32．6±1．2）mg·kg^-1·min^-1 vs （24．0±1．2）mg·kg^-1·min^-1，P〈0．01]；总胆固醇、高密度脂蛋白胆固醇则较质粒注射前明显降低[（2．36±0．22）mmol／L vs （1．60±0．21）mmol／L和（1．41±0．24）mmol／L vs（0．88±0．11）mmol／L，均P〈0．05]；在转染前后基础血糖和胰岛素水平无明显变化。结论内脂素质粒转染使IR大鼠血浆内脂素水平升高，胰岛素敏感性增强。展开更多
文摘Objective:Because children with congenital hyperinsulinism(HI) caused by recessive loss of function mutations in the adenosine triphosphate (ATP)-dependent potassium channel(KATP-HI) are not leucine sensitive,we evaluated for protein induced hypoglycemia with oral protein tolerance tests. Study design:Blood glucose and insulin concentrations were measure devery 15 minutes for 3 hours after an oral protein loadin children with KATP-HI (n=11) and compared with those of children with glutamate dehydrogenase HI (n=12) and control subjects (n=12). Results:Similar to children with glutamate dehydrogenase HI,patients with KATP-HI displayed protein-induced hypoglycemia (10/11)with blood glucose concentrations declining by 17 to 69 mg/dL. In contrast,oral proteinhad little effect on blood glucose concentrations in control subjects.Conclusions:Protein induced hypoglycemia is a feature of KATP-HI,despite the absence of leucine sensitivity. The results indicate that amino acids can stimulate insulin secretionvia a glutamate dehydrogenase and KATP channel-independent pathway.
文摘目的探讨内脂素基因过表达对高脂诱导胰岛素抵抗（IR）大鼠胰岛素敏感性的影响。方法构建大鼠内脂素基因真核表达质粒，并用该质粒转染高脂喂养诱导的IR大鼠模型。在转染前后采用两次高胰岛素-正糖钳夹技术评价大鼠胰岛素敏感性的变化。结果成功构建了内脂素真核表达载体pcDNA3．1内脂素。实验组大鼠在pcDNA3．1内脂素质粒注射后3d血浆内脂素水平较注射前明显升高（2．19±0．36 vs 0．98±0．27，P〈0．01）；在两次胰岛素钳夹中，pcDNA3．1内脂素质粒注射后葡萄糖输注率较注射前明显升高[（32．6±1．2）mg·kg^-1·min^-1 vs （24．0±1．2）mg·kg^-1·min^-1，P〈0．01]；总胆固醇、高密度脂蛋白胆固醇则较质粒注射前明显降低[（2．36±0．22）mmol／L vs （1．60±0．21）mmol／L和（1．41±0．24）mmol／L vs（0．88±0．11）mmol／L，均P〈0．05]；在转染前后基础血糖和胰岛素水平无明显变化。结论内脂素质粒转染使IR大鼠血浆内脂素水平升高，胰岛素敏感性增强。
