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 anti-insulin receptor antibody on hexose uptake and metabolism.
D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D002460:Cell Line; D002462:Cell Membrane / Q000378:metabolism; D003513:Cycloheximide / Q000494:pharmacology; D003864:Depression, Chemical; D005944:Glucosamine / Q000031:analogs & derivatives*; D006023:Glycoproteins / Q000096:biosynthesis; D006601:Hexoses / Q000378:metabolism; D007328:Insulin / Q000494:pharmacology; D051379:Mice; D011972:Receptor, Insulin / Q000378:metabolism*; D014415:Tunicamycin / Q000494:pharmacology*
D006023:Glycoproteins; D006601:Hexoses; D007328:Insulin; D014415:Tunicamycin; D003513:Cycloheximide; D011972:Receptor, Insulin; D005944:Glucosamine