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Reversible independent alterations in glucose transport and metabolism in cultured human cells deprived of glucose

Journal Article · · J. Cell. Physiol.; (United States)
We have measured uptake of /sup 3/H-hexoses into diploid human cells by exposing them to brief pulses of isotopic sugar during the log-growth, subconfluent-growth, and confluent-growth (contact inhibited) phases of the strain HSWP derived from human skin. /sup 3/H-deoxyglucose appears to be taken up three times faster than /sup 3/H-glucose. After exposure to /sup 3/H-glucose for longer than one minute, the cells excrete approximately 70 percent of the isotope into the medium as lactate. If lactate production (and hence excretion) is abolished by treating the cells with iodoacetic acid or dinitrofluorobenzene, neither of which inhibits transport, the uptake of /sup 3/H-glucose is found to be in fact somewhat larger than that of /sup 3/H-deoxyglucose. If cells are deprived of glucose for 24 hours, apparent uptake of /sup 3/H-glucose is enhanced 10-fold or more. This latter increase is accounted for by 2- to 3-fold enhancement of true transport plus retention of greater than 90 percent of the radioactivity, since little lactate is formed or excreted in glucose-deprived cells. Deoxyglucose, galactose, or pyruvate when present during glucose deprivation each have quantitatively different effects on the cells' capacity to produce lactate from a short pulse of glucose, but none of them prevents the enhancement of hexose transport. After restoration of 5 mM glucose to starved cells, their metabolism returns to normal (in the sense that approximately 70 percent of the glucose taken up in a pulse is again excreted as lactate), with a half-time of 0.5 hour; but the transport of hexoses returns to control levels much more slowly, with a half-time of approximately 6 hours. The two processes appear to be independently regulated.
Research Organization:
Univ. of Tennessee, Oak Ridge
OSTI ID:
7151971
Journal Information:
J. Cell. Physiol.; (United States), Journal Name: J. Cell. Physiol.; (United States) Vol. 89:1; ISSN JCLLA
Country of Publication:
United States
Language:
English