Increased adenine nucleotides in liver mitochondria after mannoheptulose injection in vivo.
Increased adenine nucleotides in liver mitochondria after mannoheptulose injection in vivo.
复制标题
体内注射甘露庚糖后肝线粒体中的腺嘌呤核苷酸增加。
DOI：
10.1016/0003-9861(86)90316-4
复制
发表时间：
1986
影响因子：
3.9
通讯作者：
Aprille,JR
中科院分区：
文献类型：
--
作者：
Tullson,PC;Aprille,JR
在成年大鼠中，甘露庚糖注射引起血清胰岛素与胰高血糖素比值的短暂降低，并伴随血清葡萄糖浓度的升高。这些效应在注射后1小时达到最大值，然后逐渐下降到正常水平。与激素变化相关的是肝线粒体腺嘌呤核苷酸含量（ATP + ADP + AMP）的急剧增加，在1小时时达到峰值，超过对照值的50%。线粒体腺嘌呤核苷酸的增加必须通过从细胞质中摄取而发生，因为整个组织的腺嘌呤核苷酸含量保持不变。线粒体的腺嘌呤核苷酸积累可能发生在最近表征的羧基白术苷不敏感转运途径上，该途径允许ATP-Mg交换pi。注射甘露庚糖后调节净摄取的实际机制尚未阐明；然而，载体的kmorvmax的变化和组织ATP/ADP比率的增加被排除为可能。与注射胰高血糖素相比，甘露庚糖引起的激素变化对基质腺嘌呤核苷酸含量的反应更大，更具有可重复性。因此，甘露庚糖治疗可能更适合作为进一步研究激素对线粒体功能影响的模型。
In adult rats, mannoheptulose injection causes a transient decrease in the serum insulin-to-glucagon ratio and a concomitant increase in serum glucose concentration. These effects attain a maximum 1 h after the injection and then decline toward normal. Correlated with the hormone changes is a dramatic increase in the adenine nucleotide content (ATP + ADP + AMP) of liver mitochondria, which peaks to over 50% of control values at 1 h. The increase in mitochondrial adenine nucleotides must occur by uptake from the cytosol, because the adenine nucleotide content of the whole tissue remains constant. The accumulation of adenine nucleotides by the mitochondria probably occurs over the recently characterized carboxyatractyloside-insensitive transport pathway that allows exchange of ATP-Mg forPi. The actual mechanism by which net uptake is regulated after mannoheptulose injection has not yet been elucidated; however, changes in theKmorVmaxof the carrier and an increase in the tissue ATP/ADP ratio were eliminated as possibilities. The increase in matrix adenine nucleotide content in response to hormone changes brought about by mannoheptulose was much greater and more reproducible than what is achieved with glucagon injection. Mannoheptulose treatment may therefore be preferable as a model for further study of hormone effects on mitochondrial function.