Early effects of streptozotocin-induced diabetes on insulin-like growth factor-I in the kidneys of growth hormone-transgenic and growth hormone-deficient dwarf mice

Exp Nephrol. 1997 Jul-Aug;5(4):337-44.

Abstract

Background: The renal growth and hyperfiltration observed in humans and animals with early diabetes might be dependent on growth hormone (GH) and insulin-like growth factor (IGF)-I. The aim of this study was to investigate the early changes in kidney IGF-I in experimental diabetes in mice transgenic for bovine GH and in genetically GH-deficient Ames dwarf mice.

Methods: At 2, 4 and 8 days after a single intraperitoneal injection with streptozotocin, animals were weighted, bled and killed; plasma was analyzed for glucose and IGF-I. IGF-I levels were determined in tissue from snap-frozen kidney and liver.

Results: Body weight decreased significantly after the induction of diabetes. Kidney weight increased significantly in GH-transgenic, but not in normal or dwarf mice. Plasma IGF-I was significantly decreased at day 2 in GH-transgenic and normal mice, while liver IGF-I was increased at day 4 in all mice. Kidney IGF-I increased significantly in normal and GH-transgenic mice and was increased more than 3-fold at day 4 in GH-transgenic mice. In dwarf mice, no kidney IGF-I was detectable.

Conclusion: The diabetes-induced increase in renal IGF-I is dependent on the presence of GH. GH deficiency may protect diabetic animals from early changes in the kidney.

Publication types

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

MeSH terms

  • Aging / blood
  • Analysis of Variance
  • Animals
  • Blood Glucose / metabolism
  • Cattle
  • Diabetes Mellitus, Experimental / blood
  • Diabetes Mellitus, Experimental / physiopathology*
  • Dwarfism / genetics*
  • Growth Hormone / biosynthesis*
  • Growth Hormone / deficiency*
  • Growth Hormone / genetics
  • Humans
  • Insulin-Like Growth Factor I / analysis
  • Insulin-Like Growth Factor I / biosynthesis*
  • Insulin-Like Growth Factor I / metabolism
  • Kidney / metabolism
  • Kidney / physiopathology
  • Liver / metabolism
  • Liver / physiopathology
  • Male
  • Mice
  • Mice, Mutant Strains
  • Mice, Transgenic
  • Phosphoenolpyruvate Carboxykinase (GTP) / biosynthesis
  • Phosphoenolpyruvate Carboxykinase (GTP) / genetics
  • Promoter Regions, Genetic
  • Rats
  • Recombinant Fusion Proteins / biosynthesis

Substances

  • Blood Glucose
  • Recombinant Fusion Proteins
  • Insulin-Like Growth Factor I
  • Growth Hormone
  • Phosphoenolpyruvate Carboxykinase (GTP)