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泌乳大鼠乳腺中的乳糖和脂肪酸合成。饥饿、重新喂食以及胰岛素、肾上腺素、链脲佐菌素和2-溴-α-麦角隐亭给药的影响。

Lactose and fatty acid synthesis in lactating-rat mammary gland. Effects of starvation, re-feeding, and administration of insulin, adrenaline, streptozotocin and 2-bromo-alpha-ergocryptine.

作者信息

Bussmann L E, Ward S, Kuhn N J

出版信息

Biochem J. 1984 Apr 1;219(1):173-80. doi: 10.1042/bj2190173.

Abstract

Lactose synthesis and fatty acid synthesis in intact lactating-rat mammary gland were measured simultaneously by incorporation of [U-14C]glucose and of both [U-14C]glucose and 3H2O respectively. Both processes were almost abolished by overnight starvation. Self-re-feeding caused recovery of lipogenesis to 100% of normal by 2 h and to 170% by 5 h. Lactose synthesis recovered to 80% of normal by 5 h. Food intubated to starved rats caused partial recovery in 3 h, standard diet favouring lactose synthesis and sugars favouring lipogenesis. Casein and starch were ineffective. Olive oil intubated to fed rats suppressed lipogenesis greatly and lactose synthesis slightly. Paraffin oil or water partly mimicked these effects. Adrenaline (subcutaneous) decreased lipogenesis from glucose, whereas insulin (subcutaneous) caused hypoglycaemia associated with loss of lactose synthesis but unchanged fatty acid synthesis. Streptozotocin and 2-bromo-alpha-ergocryptine (CB-154) impaired lipogenesis but not lactose synthesis. The results are interpreted in terms of competition for intracellular glucose by biosynthetic pathways for lactose and fat, and the possible implications for variations in milk composition are discussed.

摘要

通过分别掺入[U-¹⁴C]葡萄糖以及[U-¹⁴C]葡萄糖和³H₂O,同时测定完整泌乳大鼠乳腺中的乳糖合成和脂肪酸合成。这两个过程在禁食过夜后几乎都被消除。自行进食导致脂肪生成在2小时内恢复到正常水平的100%,在5小时内恢复到170%。乳糖合成在5小时内恢复到正常水平的80%。给饥饿大鼠插管喂食在3小时内导致部分恢复,标准饮食有利于乳糖合成,糖类有利于脂肪生成。酪蛋白和淀粉无效。给喂食大鼠插管橄榄油可大大抑制脂肪生成,轻微抑制乳糖合成。石蜡油或水部分模拟了这些作用。肾上腺素(皮下注射)减少了葡萄糖的脂肪生成,而胰岛素(皮下注射)导致低血糖,伴有乳糖合成减少但脂肪酸合成不变。链脲佐菌素和2-溴-α-麦角隐亭(CB-154)损害脂肪生成但不影响乳糖合成。根据乳糖和脂肪生物合成途径对细胞内葡萄糖的竞争对结果进行了解释,并讨论了其对乳汁成分变化的可能影响。

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