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Regulation of hexose transport in BALB/c 3T3 preadipose cells: Effects of glucose concentration and 12‐O‐tetradeconoylphorbol‐13‐acetate
Author(s) -
O'Brien Thomas G.,
Saladik Douglas
Publication year - 1982
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041120311
Subject(s) - cycloheximide , hexose , glucose transporter , insulin , chemistry , carbohydrate metabolism , glucose uptake , cell culture , deoxyglucose , biochemistry , 3t3 cells , tetradecanoylphorbol acetate , metabolism , biology , endocrinology , protein biosynthesis , enzyme , transfection , genetics , protein kinase c , gene
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.