Studies of acute effects of insulin-like growth factors I and II in human fat cells

J Clin Endocrinol Metab. 1987 Oct;65(4):732-7. doi: 10.1210/jcem-65-4-732.


The acute metabolic effects and receptor binding of insulin-like growth factors (IGFs) I and II were studied in human adipose tissue. The IGFs inhibited fat cell glycerol release and stimulated adipocyte 3-O-methylglucose transport and adipose tissue glucose oxidation as effectively as did insulin, but the biological potencies of the IGFs, on a molar basis, were 600-1000 times less than that of insulin. The insulin dose-response curve for antilipolysis gradually shifted to the left in the presence of submaximally and maximally effective IGF-I concentrations, whereas no additive response was found when fat cells were incubated with maximally effective concentrations of insulin and the IGFs. Adipocyte [125I]IGF-I and -II binding was low and was not inhibited by excess unlabeled IGF. In contrast, IGF-I inhibited [125I]insulin binding with a molar potency 1600 times lower than that of native insulin. In adipose tissue segments obtained from patients with untreated noninsulin-dependent diabetes mellitus, IGF-I and insulin inhibited glycerol release in a normal way. Conversely, neither insulin nor IGF-I increased the rate of glucose oxidation significantly above the nonhormone-stimulated level. We conclude that human fat cells lack specific cell surface IGF-binding sites. However, the IGFs definitely produce acute insulin-like effects in the human adipocyte, which seems to be mediated via the insulin receptor.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / drug effects*
  • Adipose Tissue / metabolism
  • Adult
  • Binding Sites / drug effects
  • Diabetes Mellitus, Type 2 / pathology
  • Female
  • Glucose / metabolism
  • Humans
  • In Vitro Techniques
  • Insulin-Like Growth Factor I / metabolism
  • Insulin-Like Growth Factor I / pharmacology*
  • Insulin-Like Growth Factor II / metabolism
  • Insulin-Like Growth Factor II / pharmacology
  • Lipolysis / drug effects
  • Male
  • Receptor, Insulin / metabolism
  • Receptors, Somatomedin
  • Somatomedins / pharmacology*


  • Receptors, Somatomedin
  • Somatomedins
  • Insulin-Like Growth Factor I
  • Insulin-Like Growth Factor II
  • Receptor, Insulin
  • Glucose