禁食大鼠大脑中钙含量及Ca(2+)-ATP酶活性的增加：与不同年龄的比较。

Increase in calcium content and Ca(2+)-ATPase activity in the brain of fasted rats: comparison with different ages.

作者信息

Hanahisa Y, Yamaguchi M

机构信息

Laboratory of Endocrinology and Molecular Metabolism, Graduate School of Nutritional Sciences, University of Shizuoka, Japan.

出版信息

Mol Cell Biochem. 1997 Jun;171(1-2):127-32. doi: 10.1023/a:1006852404215.

DOI:10.1023/a:1006852404215

PMID:9201705

Abstract

The effect of fasting on calcium content and Ca(2+)-ATPase activity in the brain tissues of 5 weeks and 50 weeks old rats was investigated. Brain calcium content and Ca(2+)-ATPase activity in the microsomal and mitochondrial functions of the brain homogenate from young and elderly rats were significantly increased by overnight-fasting. These increases were appreciably restored by a single oral administration of glucose solution (400 mg/100 g body weight) to fasted rats. In comparison with young and elderly rats, brain calcium content and microsomal Ca(2+)-ATPase activity were significantly elevated by increasing ages. The effect of ageing was not seen in the brain mitochondrial Ca(2+)-ATPase activity. When calcium (50 mg/100 g) was orally administered to young and elderly rats, brain calcium content was significantly elevated. The calcium administration-induced increase in brain calcium content was greater in elderly rats than in young rats. Also, calcium administration caused a significant increase in Ca(2+)-ATPase activity in the microsomal and mitochondrial fractions of brain homogenates from young rats. In aged rats, the microsomal Ca(2+)-ATPase activity was not further enhanced by calcium administration, although the mitochondrial enzyme activity was significantly raised. The present study demonstrates that the fasting-induced increase in brain calcium content is involved in Ca(2+)-ATPase activity raised in the brain microsomes and mitochondria of rats with different ages, supporting a energy-dependent mechanism in brain calcium accumulation.

摘要

研究了禁食对5周龄和50周龄大鼠脑组织钙含量及Ca(2+)-ATP酶活性的影响。禁食一夜后，幼龄和老龄大鼠脑匀浆微粒体和线粒体功能中的脑钙含量及Ca(2+)-ATP酶活性显著增加。给禁食大鼠单次口服葡萄糖溶液（400mg/100g体重）后，这些增加明显恢复。与幼龄和老龄大鼠相比，随着年龄增长，脑钙含量和微粒体Ca(2+)-ATP酶活性显著升高。脑线粒体Ca(2+)-ATP酶活性未出现衰老效应。给幼龄和老龄大鼠口服钙（50mg/100g）后，脑钙含量显著升高。老龄大鼠钙给药诱导的脑钙含量增加幅度大于幼龄大鼠。此外，钙给药导致幼龄大鼠脑匀浆微粒体和线粒体部分的Ca(2+)-ATP酶活性显著增加。在老龄大鼠中，尽管线粒体酶活性显著升高，但钙给药并未进一步增强微粒体Ca(2+)-ATP酶活性。本研究表明，禁食诱导的脑钙含量增加与不同年龄大鼠脑微粒体和线粒体中Ca(2+)-ATP酶活性升高有关，支持脑钙积累中的能量依赖机制。