[Study on the mechanism of hepatocytic insulin signal transduction defects in severely scalded rats].

Abstract

OBJECTIVE:

To investigate the mechanism of hepatocytic insulin signal transduction defects in severely scalded rats, so as to clarify the molecular basis of postburn insulin resistance.

METHODS:

Wistar rats inflicted by 30% III degree scalding on the back were employed as the model. The rat hepatocytic insulin receptor was partially purified by wheat-germ agglutinin (WGA)-sepharose 4B affinity chromatography. The change of receptor tyrosine protein kinase (TPK) activity, the receptor beta-subunit autophosphorylation and the hepatocytic insulin receptor binding behavior of scalded rats during early stage of scalding were observed by means of insulin receptor binding test, sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) autoradiography of phosphorylation of insulin receptor and phosphorylation of exogenous substrate.

RESULTS:

There exhibited no evident changes of hepatocytic insulin receptor maximal binding capacity and affinity at 3 postburn days (PBDs) in scalded rats. The autophosphorylation capacity of the receptor beta-subunit decreased significantly. And the receptor TPK activity decreased obviously and its reaction to insulin stimulation decreased markedly.

CONCLUSION:

The defects of the insulin receptor signal transduction in hepatocyte leading to the post-receptor defects of insulin biological effects might be molecular mechanism of postburn insulin resistance.

• Authors: Bo Zhang, Linshui Xu, Weiling Fu
• Journal: Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns (Zhonghua Shao Shang Za Zhi) Vol. 18 Issue 4 Pg. 220-2 (Aug 2002) ISSN: 1009-2587 [Print] China
• PMID: 12467533 (Publication Type: English Abstract, Journal Article)

Chemical References

• Insulin
• Receptor, Insulin

Topics

• Animals
• Burns (metabolism, pathology, physiopathology)
• Disease Models, Animal
• Hepatocytes (metabolism)
• Insulin (physiology)
• Insulin Resistance (physiology)
• Phosphorylation
• Rats
• Rats, Wistar
• Receptor, Insulin (metabolism)
• Signal Transduction (physiology)