Tunicamycin‐mediated depletion of insulin receptors in 3T3‐L1 adipocytes

Tunicamycin, an antibiotic that inhibits protein glycosylation, elicited a rapid depletion of insulin binding activity at the surface of 3T3‐L1 adipocytes. Disappearance of insulin receptors occurred more rapidly in the presence of tunicamycin than when protein synthesis was inhibited by cycloheximide and was accompanied by a diminution in sensitivity of the adipocytes to the acute effects of insulin and anit‐insulin receptor antibody on hexose uptake and metabolism.