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Hepatic insulin resistance during chronic hyperdynamic sepsis.
G C Zenni1, M P McLane, W R Law
1Department of Surgery, Loyola University Stritch School of Medicine, Maywood, IL 60153.
Circulatory Shock
|July 1, 1992
Summary
Sepsis causes hepatic insulin resistance, meaning the liver doesn't respond to insulin's glucose-lowering effects. This study demonstrates this unresponsiveness in a chronic sepsis model, impacting glucose metabolism.
Area of Science:
- Metabolic Medicine
- Physiology
- Sepsis Research
Background:
- Sepsis is associated with hyperglycemia and insulin resistance in muscle and whole body.
- Hepatic insulin resistance in sepsis remains incompletely understood.
Purpose of the Study:
- To investigate and characterize hepatic insulin resistance during chronic hyperdynamic sepsis.
Main Methods:
- A canine model of chronic hyperdynamic sepsis was established.
- Hyperinsulinemic-euglycemic clamps were performed to assess hepatic insulin sensitivity.
- Hepatic blood flow, glucose, and lactate outputs were measured.
Main Results:
- Septic animals exhibited no decrease in net hepatic glucose output (NHGO) with increasing insulin levels, indicating unresponsiveness.
- Mean arterial blood pressure decreased with insulin infusion in septic animals, unlike controls.
- Septic animals showed altered basal hepatic lactate output.
Conclusions:
- Chronic hyperdynamic sepsis induces significant hepatic insulin resistance (unresponsiveness).
- The liver's inability to suppress glucose production in response to insulin is a key feature of sepsis-induced metabolic derangement.