Regulation of hexose transport in BALB/c 3T3 preadipose cells: effects of glucose concentration and 12-O-tetradecanoylphorbol-13-acetate.

Regulation of hexose transport in BALB/c 3T3 preadipose cells: effects of glucose concentration and 12-O-tetradecanoylphorbol-13-acetate.
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BALB/c 3T3 前脂肪细胞中己糖转运的调节:葡萄糖浓度和 12-O-十四烷酰佛波醇-13-乙酸酯的影响。

DOI:
10.1002/jcp.1041120311
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发表时间:
1982
影响因子:
5.6
通讯作者:
Saladik,D
Saladik,D
中科院分区:
生物学2区
文献类型:
--
作者:
O'Brien,TG;Saladik,D

文献摘要

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与培养的许多细胞类型一样,未分化和分化的BALB/c 3T3前体脂肪细胞对葡萄糖缺乏的反应是摄取2-脱氧-D-葡萄糖(脱氧葡萄糖)和3-O-甲基-D-葡萄糖(甲基葡萄糖)。将葡萄糖重新加入无糖培养物可导致摄取活性迅速下降;在未分化的细胞中,葡萄糖的半最大有效浓度约为0.5 mM,而0.1 mM则无效。几种己糖在缺糖细胞中“抑制”甲基葡萄糖运输的效果不同;似乎特定的己糖必须代谢超过6-磷酸才能使运输系统失活。以往的研究表明佛波酯12-O-十四酰佛波醇-13-乙酸酯(TPA)能刺激未分化和分化的BALB/c 3T3细胞的己糖转运。在这项研究中,发现TPA(和分化细胞中的胰岛素)阻止了葡萄糖诱导的转运蛋白活性的失活。与葡萄糖同时加入放线菌素D或放线菌素D也可防止葡萄糖引起的转运活性失活。在葡萄糖缺乏的细胞中,TPA和胰岛素等药物似乎超越了对外部葡萄糖浓度敏感的细胞控制机制,因此在通常会导致运输活性下降的环境条件下(即恢复到生理葡萄糖浓度),运输活动的水平保持在较高水平。
Like many cell types in culture, both undifferentiated and differentiated BALB/c 3T3 preadipose cells respond to glucose deprivation with an increased uptake of 2‐deoxy‐D‐glucose (deoxyglucose) and 3‐O‐methyl‐D‐glucose (methylglucose). Glucose readdition to glucose‐deprived cultures resulted in a prompt fall in uptake activity; in undifferentiated cells, a half‐maximally effective concentration of glucose was approximately 0.5 mM, while 0.1 mM was ineffective. Several hexoses differed in their efficacy of “deactivating” methylglucose transport in glucose‐deprived cells; it appeared that a particular hexose must be metabolized beyond the 6‐phosphate from to deactivate the transport system. Previous studies have shown that the phorbol ester 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) stimulates hexose transport in undifferentiated and differentiated BALB/c 3T3 cells. In this study, it was found that TPA (and insulin in differentiated cells) prevented the glucose‐induced deactivation of transport activity. Glucose‐induced deactivation of transport activity was also prevented by cycloheximide or actinomycin D addition concomitantly with glucose. In glucose‐starved cells, agents such as TPA and insulin appear to override a cellular control mechanism sensitive to the external concentration of glucose, so that elevated levels of transport activity are maintained under environmental conditions (i.e., a return to physiological glucose concentrations) that normally induce a fall in transport activity.