Insulin induction of c-Ki-ras in rat liver and in cultured normal rat hepatocytes

Comp Biochem Physiol B. 1993 Feb;104(2):341-7. doi: 10.1016/0305-0491(93)90377-h.

Abstract

1. Insulin administration in neonatal rats causes a dramatic accumulation of the major c-Ki-ras transcript. 2. The level of c-Ki-ras transcript is greatly reduced in alloxan-induced diabetic rats. 3. Injection of insulin in alloxan-induced diabetic rats is able to restore almost completely the level of c-Ki-ras transcript found in insulin-induced normal rats. 4. Results from nuclear run-off experiments reveal that the inductive effect of insulin is at the level of transcription of the c-Ki-ras gene. 5. As in whole animals, insulin is also able to induce the expression of c-Ki-ras in cultured normal hepatocytes. 6. This inductive effect of insulin is markedly reduced in hepatocytes which have been previously treated with the tumour promoter, 12-O-tetradecanoylphorbol-13 acetate for 24 hr, a result suggesting that at least part of the effect of insulin is mediated via protein kinase C.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging / metabolism
  • Animals
  • Cells, Cultured
  • Diabetes Mellitus, Experimental / metabolism
  • Enzyme Activation
  • Gene Expression / drug effects*
  • Insulin / pharmacology*
  • Liver / cytology
  • Liver / drug effects
  • Liver / metabolism*
  • Protein Kinase C / metabolism
  • Proto-Oncogene Proteins p21(ras) / biosynthesis*
  • Proto-Oncogene Proteins p21(ras) / genetics
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Tetradecanoylphorbol Acetate / pharmacology
  • Transcription, Genetic / drug effects
  • Tumor Cells, Cultured

Substances

  • Insulin
  • RNA, Messenger
  • Protein Kinase C
  • Proto-Oncogene Proteins p21(ras)
  • Tetradecanoylphorbol Acetate