Glucose starvation alters insulin but not IGF-I binding to Chinese hamster ovary (CHO) cells.
The pattern of cellular protein glycosylation can be altered in CHO cells by glucose starvation. When wild type CHO cells are deprived of glucose, 125I-insulin binding increases from a B/F of 0.033 +/- 0.004 to 0.063 +/- 0.011, due to an increase in receptor affinity. The already elevated insulin binding to mutant B4-2-1 CHO cells, whose genetic defect causes abnormal glycosylation mimicking the pattern seen in the glucose starved normal cells, is not affected by glucose starvation. In neither cell line is 125I-IGF-I binding affected by glucose starvation. These data support the hypothesis that abnormal glycosylation can alter insulin binding to its receptor. Furthermore, there is a striking difference in the susceptibility of IGF-I and insulin receptors to alterations in glycosylation.
D000818:Animals; D002460:Cell Line; D005947:Glucose / Q000502:physiology*; D007328:Insulin / Q000378:metabolism*; D007334:Insulin-Like Growth Factor I / Q000378:metabolism*; D009154:Mutation; D011869:Radioligand Assay; D011972:Receptor, Insulin / Q000378:metabolism*; D013002:Somatomedins / Q000378:metabolism*
D007328:Insulin; D013002:Somatomedins; D007334:Insulin-Like Growth Factor I; D011972:Receptor, Insulin; D005947:Glucose