GONADAL STEROID EFFECT ON MYOFIBRILLAR PROTEIN SYNTHESIS

以前的研究表明，健康的老年人有较慢的速度， 肌原纤维蛋白质的合成比年轻的成年人。 这种蛋白质的变化 合成可能对肌肉质量和功能产生不利影响。 恢复更年轻的肌原纤维蛋白合成速率 可能有助于最大限度地减少肌肉萎缩相关的 衰老 因为老化也与减少生产有关， 因为有证据表明性腺类固醇 可能对肌肉产生合成代谢作用，将进行研究， 性腺激素替代对肌原纤维蛋白代谢的影响 60岁以上的健康志愿者。 这些研究旨在测试 几种假设：睾酮替代刺激肌原纤维 非SHBG结合睾酮水平低的男性的蛋白质合成; 阻断睾酮向二氢睾酮的转化 抑制睾酮对双氢睾酮的合成代谢作用 不抑制睾酮的合成代谢作用;雌激素替代品 刺激绝经后妇女的肌原纤维蛋白合成; 沿着雌激素替代物的给予能减弱这种效应 睾酮刺激肌原纤维蛋白合成 绝经后妇女（剂量小于男性）; 性腺类固醇增加了组织中编码 丰富的肌原纤维蛋白。 肌原纤维蛋白质的合成 通过掺入稳定同位素示踪剂测定。 肌纤维 降解将通过3-甲基组氨酸排泄测定。 水平 mRNA将通过将肌肉RNA与特异性反义核酸杂交来测定。 RNA探针。 本研究中获得的基本知识有助于 阐明性腺类固醇是否可以作为 预防或逆转老年肌肉萎缩的综合策略。

Previous research shows that healthy older people have slower rates of myofibrillar protein synthesis than young adults. This change in protein synthesis could have adverse effects on muscle mass and function. Restoring a more youthful rate of myofibrillar protein synthesis potentially could help to minimize the muscle atrophy associated with aging. Because aging also is associated with decreased production of gonadal steroids, and because there is evidence that gonadal steroids could have anabolic effects in muscle, studies will be done to examine the effects of gonadal steroid replacement on myofibrillar protein metabolism in healthy volunteers over 60 years old. The studies are designed to test several hypotheses: that testosterone replacement stimulates myofibrillar protein synthesis in men with low non-SHBG-bound testosterone levels; that blocking conversions of testosterone to dihydrotestosterone does not inhibit the anabolic effect of testosterone to dihydrotestosterone does not inhibit the anabolic effect of testosterone; that estrogen replacement stimulates myofibrillar protein synthesis in postmenopausal women; that giving progestin along with the estrogen replacement attenuates the effect of estrogen; that testosterone stimulates myofibrillar protein synthesis in postmenopausal women (with a smaller dose than that given to men); that gonadal steroids increase tissue levels of the mRNAs that encode the abundant myofibrillar proteins. Myofibrillar protein synthesis will be determined by incorporation of a stable isotope tracer. Myofibrillar degradation will be determined by 3-methylhistidine excretion. Levels of mRNAs will be determined by hybridizing muscle RNA with specific antisense RNA probes. The basic knowledge gained in this study could help to elucidate whether gonadal steroids could be useful as part of a comprehensive strategy to prevent or reverse muscle atrophy in old age.