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首页> 外文期刊>The biochemical journal >Evidence that the stimulation of lipogenesis in the mammary glands of starved lactating rats re-fed with a chow diet is dependent on continued hepatic gluconeogenesis during the absorptive period. Effects of a gluconeogenic inhibitory, mercaptopicolinic acid, in vivo
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Evidence that the stimulation of lipogenesis in the mammary glands of starved lactating rats re-fed with a chow diet is dependent on continued hepatic gluconeogenesis during the absorptive period. Effects of a gluconeogenic inhibitory, mercaptopicolinic acid, in vivo

机译:有证据表明,用Chow饮食重新喂养的饥饿乳酸大鼠的乳腺乳腺刺激依赖于吸收期间的持续肝糖生成。葡糖原抑制,巯基胆碱酸,体内的影响

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pThe rapid stimulation of lipogenesis in mammary gland that occurs on re-feeding starved lactating rats with a chow diet was decreased (60%) by injection of mercaptopicolinic acid, an inhibitor of hepatic gluconeogenesis at the phosphoenolpyruvate carboxykinase step. Mercaptopicolinate had no effect on lipogenesis in mammary glands of fed lactating rats. The inhibition of lipogenesis persisted in vitro when acini from mammary glands of re-fed rats treated with mercaptopicolinate were incubated with [1-14C]glucose. Mercaptopicolinate added in vitro had no significant effect on lipogenesis in acini from starved-re-fed lactating rats. Mercaptopicolinate prevented the deposition of glycogen and increased the rate of lipogenesis in livers of starved-re-fed lactating rats, whereas it had no significant effect on livers of fed lactating rats. Administration of intraperitoneal glucose restored the rate of mammary-gland lipogenesis in re-fed rats treated with mercaptopicolinate to the values for re-fed rats. Hepatic glycogen deposition was also restored, and the rate of hepatic lipogenesis was stimulated 5-fold. It is concluded that stimulation of mammary-gland lipogenesis on re-feeding with a chow diet after a period of starvation is in part dependent on continued hepatic gluconeogenesis during the absorptive period. Possible sources of the glucose precursors are discussed./p
机译:>通过注射磷酸丙烯酸甲基酶甲基酶步骤中,通过注射磷酸胆糖醇(60%)在再喂食饥饿的乳酸大鼠中发生乳腺癌的快速刺激。巯基因素对哺乳动物大鼠乳腺脂肪发生没有影响。将脂肪生成的抑制在体外持续存在,当用巯基胆碱处理的重新喂养大鼠的乳腺腺体含有[1-14℃]葡萄糖时,抑制含有乳腺腺体。在体外添加的巯基胆碱酸盐对来自氟化术乳酸大鼠的Acini中的脂肪生成没有显着影响。巯基胆碱可防止糖原的沉积并增加血液乳蛋白乳腺癌肝脏中的脂肪生成率,而对哺乳酸大鼠的肝脏没有显着影响。腹膜内葡萄糖的施用恢复了用巯基丙酮酸盐处理的再喂养大鼠的乳腺腺体脂肪生成的速率恢复到重新喂养大鼠的值。还恢复肝糖原沉积,肝脂肪生成的速率刺激5倍。结论是,在饥饿期后,刺激乳腺脂肪发生在用味道饮食再喂养,部分依赖于吸收期间继续肝葡糖生成。讨论了葡萄糖前体的可能源。

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