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(Chest. 1975;67:60S-63S.)
© 1975 American College of Chest Physicians

Factors in Glucose Oxidation by Alveolar Macrophages

Glucose Transport and Glycogenolysis

Atul S. Khandwala Ph.D.1 and J. Bernard L. Gee M.D.1

1 Yale University Lung Research Center, Yale University School of Medicine, New Haven

2DG transport rate is 0.135 ± 0.013 nmoles 2DG transported/minute/l06 AM at 8 mM external 2DG concentration. The minimal rates of glucose utilization are 0.04 and 0.20 nmoles/minute/106 AM in resting and phagocytosing AM respectively.6 This conversion rate represents a minimal rate for glucose utilization since other glucose utilization pathways are not measured by measurement of CO2 production from glucose. Thus, if the measured 2DG transport rate reasonably reflects the glucose transport rate, then pharmacologic impairment of transport will prove to be rate limiting for metabolism. Our studies with cytochalasin B and similar ones with other cell types are most readily explained in this manner. Our observations with the phosphodiesterase inhibitor, theophylline, which inhibits both 2DG transport and glucose conversion to CO2, by 40 to 60 percent, suggest that impaired glucose transport is an important factor in inhibiting glucose metabolism by AM and perhaps other phagocytes. The impaired transport assumes considerable importance in phagocytosing AM in which glucose conversion to CO2, increases up to 5-fold.







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Copyright © 1975 by the American College of Chest Physicians.