Skeletal muscle insulin resistance during Escherichia coli bacteremic shock in the dog.

Abstract

Skeletal muscle glucose uptake during close, intra-arterial insulin infusion was studied before and during live Escherichia coli bacteremic shock in the dog. An in vivo, constant-flow perfused gracilis muscle preparation was used. Insulin infusion before shock resulted in a 395% increase in muscle glucose uptake, which was independent of changes in muscle lactate production or oxygen uptake. At 1, 2, and 3 hours of shock, insulin infusion had no effect on gracilis muscle glucose uptake. This loss of responsiveness to insulin occurred with no change in muscle oxygen uptake, muscle venous PO2, or muscle blood flow (held constant). On the other hand, during nonshock control experiments, muscle glucose uptake in response to insulin infusion was maintained during the 3-hour protocol. These data demonstrate that skeletal muscle insulin resistance develops early during bacteremic shock.

• Authors: R M Raymond, J M Harkema, T E Emerson Jr
• Journal: Surgery (Surgery) Vol. 90 Issue 5 Pg. 853-9 (Nov 1981) ISSN: 0039-6060 [Print] United States
• PMID: 7029767 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Lactates
• Lactic Acid
• Glucose

Topics

• Animals
• Dogs
• Escherichia coli Infections (physiopathology)
• Female
• Glucose (metabolism)
• Insulin Resistance
• Lactates (metabolism)
• Lactic Acid
• Male
• Muscles (drug effects, metabolism)
• Oxygen Consumption
• Shock, Septic (physiopathology)
• Time Factors