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Am J Physiol Gastrointest Liver Physiol (September 25, 2002). doi:10.1152/ajpgi.00217.2002
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Articles in PresS, published online ahead of print September 25, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00217.2002
Submitted on June 7, 2002
Accepted on September 10, 2002

Hemorrhage Induces The Rapid Development of Hepatic Insulin Resistance

Yuchen Ma1, Ping Wang2, Joachim F. Kuebler3, Irshad H. Chaudry4, and Joseph L. Messina1*

1 Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA
2 Center for Surgical Research and Department of Surgery, University of Alabama at Birmingham, Birmingham, AL, USA; Department of Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, AL, USA; Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA
3 Center for Surgical Research and Department of Surgery, University of Alabama at Birmingham, Birmingham, AL, USA
4 Center for Surgical Research and Department of Surgery, University of Alabama at Birmingham, Birmingham, AL, USA; Department of Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, AL, USA

* To whom correspondence should be addressed. E-mail: messina{at}path.uab.edu.

Hyperglycemia is an early metabolic response to trauma and hemorrhage. The role of hepatic insulin resistance to the development of this hyperglycemia is not well understood. The aim of this study was to determine whether the liver becomes insulin resistant and to identify the particular hepatic insulin signaling pathways that may be compromised following trauma and hemorrhage. Male adult rats were bled to a mean arterial pressure of 40 mmHg and maintained at that pressure for 90 min followed by resuscitation with Ringer's lactate. Data showed that trauma and hemorrhage rapidly induced profound hyperinsulinemia in combination with significant hyperglycemia, suggesting the development of insulin resistance. Following trauma and hemorrhage, hepatic insulin signaling via the insulin-induced PI-3 kinase (phosphatidyl-inositol-3 kinase)-Akt signaling was abolished, while ERK1/2 (extracellular signal regulated kinase) pathway was relatively normal. The regulation (inhibition) of a hepatic, insulin and PI-3 kinase-dependent gene, IGFBP-1, was also lost. The present study provides convincing evidence of a rapid onset hepatic insulin resistance following a combination of trauma and hemorrhage.






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