Acute regulation of hepatic glutathione S-transferase by insulin and glucagon

Toxicol Lett. 1995 Mar;76(2):105-11. doi: 10.1016/0378-4274(94)03203-j.

Abstract

The intravenous administration of insulin plus glucose in anesthetized rats caused, within 30 min, an increase of about 56% in hepatic cytosolic glutathione S-transferase (GST) activity, but it did not affect the microsomal enzyme. The injection of glucagon resulted, at the same time, in a 43% drop in the hepatic cytosolic GST, without affecting the microsomal GST. The insulin-dependent increase in cytosolic GST activity was abolished by the pretreatment of the animals with an inhibitor of protein synthesis (cycloheximide). A kinetic analysis revealed a non-competitive inhibition caused by glucagon upon the cytosolic enzyme. In addition, the presence of insulin did not interfere with the effectiveness of glucagon, and vice versa. We propose that: (1) the effect of insulin on hepatic cytosolic GST activity requires protein synthesis; (2) glucagon produces an inhibition of hepatic cytosolic GST, which could be mediated by cytosolic effectors such as adenosine 3'-5'-cyclic monophosphate (cAMP); (3) the effects of glucagon and insulin were not mutually exclusive; (4) hepatic microsomal GST is regulated by different mechanism(s).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bucladesine / pharmacology
  • Cyclic AMP / physiology
  • Cycloheximide / pharmacology
  • Cytosol / enzymology
  • Glucagon / administration & dosage
  • Glucagon / physiology*
  • Glutathione Transferase / metabolism*
  • In Vitro Techniques
  • Insulin / administration & dosage
  • Insulin / physiology*
  • Liver / enzymology*
  • Male
  • Rats
  • Rats, Wistar
  • Time Factors

Substances

  • Insulin
  • Bucladesine
  • Glucagon
  • Cycloheximide
  • Cyclic AMP
  • Glutathione Transferase