Emerman J T, Bartley J C, Bissell M J
Biochem J. 1980 Nov 15;192(2):695-702. doi: 10.1042/bj1920695.
Glycogen metabolism in mammary epithelial cells was investigated (i) by studying the conversion of glucose into glycogen and other cellular products in these cells from virgin, pregnant and lactating mice and (ii) by assaying the enzymes directly involved with glycogen metabolism. We find that: (1) mammary epithelial cells synthesized glycogen at rates up to over 60% that of the whole gland; (2) the rate of this synthesis was modulated greatly during the reproductive cycle, reaching a peak in late pregnancy and decreasing rapidly at parturition, when abundant synthesis of lactose was initiated; (3) glycogen synthase and phosphorylase activities reflected this modulation in glycogen metabolism; (4) lactose synthesis reached a plateau during late pregnancy, even though lactose synthase is reported to increase in the mouse mammary gland at this time. We propose that glycogen synthesis restricts lactose synthesis during late pregnancy by competing successfully for the shared UDP-glucose pool. The physiological advantage of glycogen accumulation during late pregnancy is discussed.
(i)研究来自处女、怀孕和哺乳期小鼠的这些细胞中葡萄糖向糖原及其他细胞产物的转化;(ii)测定直接参与糖原代谢的酶。我们发现:(1)乳腺上皮细胞合成糖原的速率高达全腺合成速率的60%以上;(2)这种合成速率在生殖周期中受到极大调节,在妊娠后期达到峰值,并在分娩时迅速下降,此时开始大量合成乳糖;(3)糖原合酶和磷酸化酶活性反映了糖原代谢中的这种调节;(4)尽管据报道此时小鼠乳腺中的乳糖合酶增加,但乳糖合成在妊娠后期达到平台期。我们提出,在妊娠后期糖原合成通过成功竞争共享的UDP-葡萄糖池来限制乳糖合成。讨论了妊娠后期糖原积累的生理优势。