嘌呤霉素对培养脂肪组织的影响及其对地塞米松、胰岛素和肾上腺素的反应

John N. Fain
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引用次数: 27

摘要

1.1. Puromycin(10−4 M)、Puromycin氨基核苷(10−4 M)和地塞米松(4·10−8 M)降低了培养大鼠脂肪组织对葡萄糖的吸收和向CO2、甘油-甘油和脂肪酸的转化。这些物质对脂肪组织对果糖或丙酮酸的代谢几乎没有影响。嘌呤霉素阻断或减少葡萄糖、果糖和丙酮酸碳与蛋白质的结合;氨基核苷和地塞米松作用小。Puromycin阻断胰岛素对蛋白质合成的刺激,但不改变胰岛素的其他作用,也不改变地塞米松和肾上腺素对脂肪组织的作用。在嘌呤霉素存在和不存在的情况下,胰岛素降低丙酮酸向乳酸的转化,增加其向脂肪酸的转化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of puromycin on incubated adipose tissue and its response to dexamethasone, insulin, and epinephrine

  • 1.

    1. Puromycin (10−4 M), puromycin aminonucleoside (10−4 M) and dexamethasone (4·10−8 M) decreased the uptake and conversion of glucose to CO2, glyceride-glycerol and fatty acid by incubated rat-adipose tissue. These substances had little effect on the metabolism of fructose or pyruvate by adipose tissue. Puromycin blocked or decreased the incorporation of glucose, fructose, and pyruvate carbon into protein; aminonucleoside and dexamethasone had little effect.

  • 2.

    2. Puromycin blocked the stimulation of protein synthesis by insulin but did not alter the other actions of insulin or the effects of dexamethasone and epinephrine on adipose tissue.

  • 3.

    3. Insulin decreased the conversion of pyruvate to lactate and increased its conversion to fatty acid in the presence and the absence of puromycin.

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