Dietary protein restriction inhibits growth hormone-induced DNA synthesis without impairing c-myc and c-Ha-ras expression in the liver of hypophysectomized rats

J Nutr. 1995 Jul;125(7):1847-53. doi: 10.1093/jn/125.7.1847.

Abstract

Cellular proliferation is impaired by malnutrition, and the mechanisms responsible for this inhibitory effect are poorly understood. One possible mechanism might involve alterations of the cell cycle-associated proto-oncogene expression. To test this hypothesis, we studied the effects of dietary protein restriction on DNA synthesis and c-myc and c-Ha-ras proto-oncogene mRNA responses to growth hormone in the liver of hypophysectomized rats. In rats fed a normal protein diet (15% protein), growth hormone injection induced a sequential activation of c-myc expression (13 times the baseline value, after 1 h) and c-Ha-ras expression (two times the baseline value, after 6 h), which was followed by a stimulation of liver DNA synthesis (9 times the baseline value, after 24 and 36 h). In rats fed a protein-restricted diet (5% protein), growth hormone injection did not induce liver DNA synthesis after 24 or 36 h. However, the baseline level of c-myc mRNA was higher in protein-restricted than in rats fed a normal diet and that of c-Ha-ras mRNA was unaffected by protein restriction. Furthermore, the peak response of c-myc mRNA was more important in protein-restricted rats than in rats fed a normal diet, and the c-Ha-ras mRNA response to growth hormone injection was similar in both dietary groups. These results show that dietary protein restriction inhibits growth hormone-induced DNA synthesis without impairing c-myc and c-Ha-ras activation in the liver of hypophysectomized rats.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Northern
  • Body Weight
  • Cell Division / drug effects
  • Cell Division / genetics
  • DNA / biosynthesis*
  • Diet, Protein-Restricted*
  • Female
  • Gene Expression Regulation / drug effects
  • Genes, myc
  • Genes, ras
  • Growth Hormone / pharmacology*
  • Hypophysectomy
  • Insulin-Like Growth Factor I / analysis
  • Liver / drug effects*
  • Liver / metabolism
  • Liver / physiology
  • Oncogene Protein p21(ras) / biosynthesis
  • Oncogene Protein p21(ras) / genetics*
  • Organ Size
  • Proto-Oncogene Proteins c-myc / biosynthesis
  • Proto-Oncogene Proteins c-myc / genetics*
  • RNA, Messenger / analysis
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Wistar

Substances

  • Proto-Oncogene Proteins c-myc
  • RNA, Messenger
  • Insulin-Like Growth Factor I
  • Growth Hormone
  • DNA
  • Oncogene Protein p21(ras)