Effects of caloric restriction and aging on erythrocyte membrane Ca(2+)-ATPase activity in specific pathogen-free Fischer 344 rats.
Effects of caloric restriction and aging on erythrocyte membrane Ca(2+)-ATPase activity in specific pathogen-free Fischer 344 rats.
复制标题
热量限制和衰老对特定无病原体 Fischer 344 大鼠红细胞膜 Ca(2)-ATP 酶活性的影响。
DOI：
10.1016/0026-0495(91)90009-l
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Blas,SD
中科院分区：
文献类型：
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作者：
Davis,FB;Deziel,MR;VanLiew,JB;Davis,PJ;Bernardis,LL;Blas,SD
饮食热量限制延长Fischer 344大鼠的寿命。在Fischer大鼠中，在质膜转运相关酶、Ca 2 +-腺苷三磷酸酶（ATP酶）和Na，K-ATP酶的水平上检查了衰老和热量限制的相互作用。动物分为4个年龄组，范围为6.1至25.0个月，并且无特定病原体（SPF，屏障提高）。将以随意饮食饲养的雄性和雌性动物的结果与接受其随意同窝出生仔的60%年龄特异性热量摄入的大鼠的结果进行比较。测定了红细胞膜Ca ~（2+）-ATP酶活性对甲状腺激素（T_4、T_3）和Ca ~（2+）-ATP酶激活剂钙调素（CaM）的反应。红细胞膜Na，K-ATP酶也比较了两个饮食组，是血浆葡萄糖。与自由进食的动物相比，在不添加甲状腺激素和钙调素的情况下，热量限制大鼠的质膜Ca 2 +-ATP酶活性显著降低（-39%，P < .001），并且在6.1、12.7、17.0和25.0个月的四个年龄组中的反应相似。相反，与自由活动组相比，热量限制组动物对T4和T3的Ca 2 +-ATP酶反应增强（分别为+62%和+58%，P <0.001）。在热量剥夺的动物中，该酶的钙调素反应性增加了45%（P<0.001），类似于T4和T3反应性的变化。根据年龄进行分析，发现在年轻（6个月）的动物中，钙调素对Ca 2 +-ATP酶活性的反应性的饮食相关差异最大;在13个月、17个月和25个月大的大鼠中，饮食影响减弱。饲料条件性升高T4和T3对Ca 2 +-ATP酶活性的刺激在所有年龄组中是相似的。对红细胞（RBC）Na，K-ATP酶活性无性别、年龄或饮食依赖性影响。自由进食组和限制热量组的血糖水平无显著差异。因此，Fischer 344 SPF大鼠的慢性热量限制降低了6至25月龄动物的RBC膜Ca 2 +-ATP酶活性，但不降低Na，K-ATP酶活性。与此相反，限制饮食与显着增加的Ca 2 +-ATP酶反应在体外T4，T3，和钙调素。对钙调素的增强反应在6个月龄组中最为显著。
Dietary caloric restriction extends life span in the Fischer 344 rat. The interaction of aging and caloric restriction was examined at the level of the plasma membrane transport-associated enzymes, Ca2+-adenosine triphosphatase (ATPase) and Na,K-ATPase, in the Fischer rat. Animals were in four age groups, ranging from 6.1 to 25.0 months, and were specific pathogen-free (SPF, barrier-raised). Results from male and female animals raised on an ad libitum diet were compared with those from rats that received 60% of the age-specific caloric intake of their ad lib littermates. The responses of erythrocyte membrane Ca2+-ATPase activity in vitro to thyroid hormone (l-thyroxine [T4]; 3,5,3′-triiodothyronine [T3]) and to purified calmodulin, a Ca2+-binding protein activator of Ca2+-ATPase, were measured. Erythrocyte membrane Na,K-ATPase was also compared in the two diet groups, as was plasma glucose. Plasma membrane Ca2+-ATPase activity in the absence of added thyroid hormone and calmodulin was significantly reduced in calorically restricted rats (−39%,P< .001), compared with ad lib-fed animals, and the response was similar in the four age groups aged 6.1, 12.7, 17.0, and 25.0 months. In contrast, pooled (all ages) Ca2+-ATPase response in vitro to T4and to T3in calorically restricted animals was enhanced compared with the ad lib group (+62% and +58%,P< .001, respectively). Calmodulin responsiveness of the enzyme was increased by 45% (P< .001) in calorie-deprived animals, similar to the change in T4and T3responsiveness. Analyzed on an age-specific basis, the diet-related difference in calmodulin responsiveness of Ca2+-ATPase activity was found to be greatest in young (6 months) animals; the diet effect was lessened in the 13-, 17- and 25-month-old rats. Diet-conditioned heightening of T4and T3stimulation of Ca2+-ATPase activity was similar in all age groups. There were no sex-, age-, or diet-dependent effects on red blood cell (RBC) Na,K-ATPase activity. There was no significant difference in plasma glucose levels between the ad lib and calorie-restricted animals. Thus, chronic caloric restriction in Fischer 344 SPF rats reduces RBC membrane Ca2+-ATPase, but not Na,K-ATPase, activity in animals ranging in age from 6 to 25 months. In contrast, the restricted diet was associated with significantly increased Ca2+-ATPase response in vitro to T4, T3, and calmodulin. The enhanced response to calmodulin was most marked in the 6-month age group.