Modulation of endogenous hormone action by recombinant human tumor necrosis factor. Academic Article uri icon

Overview

abstract

  • Tumor necrosis factor (TNF) has been implicated in the toxic manifestations of overwhelming bacterial infection and in the tissue wasting that often accompanies prolonged infections and malignancy. We have examined a possible role of TNF in the early metabolic alterations following acute tissue injury or sepsis. Recombinant human TNF stimulated rat liver amino acid uptake up to 5-fold in vivo and there was a concomitant increase in plasma glucagon. In vitro TNF had no direct effect on hepatocyte amino acid uptake, but it markedly enhanced the stimulation of amino acid transport by glucagon, without an alteration in binding of glucagon to hepatocytes. This permissive effect of TNF on glucagon action represents an interrelationship between the immune and endocrine systems, and it may help to explain the mechanism of hormonal regulation of both the anabolic and catabolic responses to acute injury.

publication date

  • December 1, 1987

Research

keywords

  • Amino Acids
  • Glucagon
  • Liver
  • Tumor Necrosis Factor-alpha

Identity

PubMed Central ID

  • PMC299597

Scopus Document Identifier

  • 0023546088

PubMed ID

  • 2825198

Additional Document Info

volume

  • 84

issue

  • 23