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

J Cell Physiol. 1979 Apr;99(1):37-42. doi: 10.1002/jcp.1040990106.

Abstract

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adipose Tissue / metabolism*
  • Animals
  • Cell Line
  • Cell Membrane / metabolism
  • Cycloheximide / pharmacology
  • Depression, Chemical
  • Glucosamine / analogs & derivatives*
  • Glycoproteins / biosynthesis
  • Hexoses / metabolism
  • Insulin / pharmacology
  • Mice
  • Receptor, Insulin / metabolism*
  • Tunicamycin / pharmacology*

Substances

  • Glycoproteins
  • Hexoses
  • Insulin
  • Tunicamycin
  • Cycloheximide
  • Receptor, Insulin
  • Glucosamine