cytochalasin-b and Starvation

The capacity of Ehrlich ascites tumour cells to take up 2-deoxy-D-glucose and to bind cytochalasin B varies adaptatively with the level of glucose in the plasma or culture medium. The effect of glucose is exerted directly on the cells and does not necessarily require the participation of hormones such as insulin, glucagon or corticosterone, although glucagon and the glucocorticoids, but not insulin, can also increase the number of glucose carrier molecules administered in vitro. Cycloheximide suppresses the acute inductive effect of glucose, suggesting that protein synthesis might be required for the increased transport activity.

Topics: Animals; Binding Sites; Biological Transport; Carcinoma, Ehrlich Tumor; Cycloheximide; Cytochalasin B; Deoxyglucose; Glucose; Hormones; Mice; Mice, Inbred ICR; Monosaccharide Transport Proteins; Neoplasm Proteins; Starvation

Starvation-induced hypoglycaemia and streptozotocin-induced diabetes suppressed the growth of Ehrlich ascites tumor in mice. The suppression of tumor growth by diabetes was alleviated by administration of insulin. The number of glucose carriers on tumour cells was found to be reduced in diabetes and partial resumption of glucose carriers was observed in tumour cells of diabetes after insulin administration. Insulin had no direct effect on tumour growth in vivo and did not affect the number of glucose carriers on tumour cells in vitro. The physiological significance of these observations is discussed.

Topics: Animals; Biological Transport; Blood Glucose; Carcinoma, Ehrlich Tumor; Cytochalasin B; Diabetes Mellitus, Experimental; Glucose; Insulin; Mice; Starvation

Cellular regulation of hexose uptake was studied in cultures of NIL hamster cells. Enhancements of galactose uptake were elicited most strikingly by maintaining confluent NIL cultures in culture media devoid of glucose. These glucose-starved cultures showed up to 8- or 9-fold enhancements in the galactose uptake test. When these cultures were treated for extended periods with cycloheximide, the enhanced uptake was left unimpaired, whereas the uptake by glucose-fed cells, similarly treated with cycloheximide, was inhibited greater than 90%. Addition of glucose to these starved cultures resulted in a gradual decline of uptake rates to the unenhanced level (t1/2 approximately 3 hr). In surprising contrast, when both glucose and cycloheximide were added simultaneously, the decline was arrested for at least 12 hr. If cytochalasin B (the specific inhibitor of hexose transport) was present, the uptake of galactose by both starved and fed cells was close to completely inhibited. By several criteria, cells maintained for 24 hr in medium containing both glucose and cytochalasin B were glucose-fed. Yet, when the cytochalasin B was removed, the cells were found to have enhanced rates of galactose uptake. The regulation of the hexose uptake system may therefore not be guided by the levels of glucose catabolites. Alternative mechanisms that may control hexose uptake are considered.

Topics: Biological Transport; Cells, Cultured; Cycloheximide; Cytochalasin B; Deoxyglucose; Galactose; Glucose; Kinetics; Leucine; Starvation