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Joseph F. Amaral, MD; Jeffry D. Shearer, MA; Balduino Mastrofrancesco, MS; Donald S. Gann, MD; Michael D. Caldwell, MD, PhD

Arch Surg. 1989;124(6):727-732.

Abstract
• The administration of endotoxin in vivo results in an increase in glucose utilization through an as yet undetermined mechanism. This study evaluated (1) the contribution of blood to the increased glucose utilization noted following endotoxemia, (2) the direct action of endotoxin on skeletal muscle glucose uptake in an isolated hindlimb perfusion system and in incubated muscle, and (3) the possibility that the increased glucose uptake in skeletal muscle mediated by endotoxin requires the presence of plasma. Incubation of blood with 50 and 100 mg/L of endotoxin increased glucose uptake and lactate production in a dose-dependent manner. Muscle incubations and perfusions in the absence of plasma and white blood cells showed that glucose uptake and lactate production were not affected by the presence of 50 to 250 mg/L of endotoxin, while 500 mg/L of endotoxin produced a 26.2% decrease in glucose uptake. In contrast, incubation of muscle in the presence of plasma and endotoxin increased glucose uptake by 37%. These findings suggest that (1) the increased glucose utilization of endotoxemia is only partially explained by increased glucose metabolism by blood, (2) endotoxin does not have a direct effect on the glucose uptake of skeletal muscle, and (3) an interaction of endotoxin with a component of plasma is required for an endotoxin-mediated increase in glucose utilization by skeletal muscle.

(Arch Surg 1989;124:727-732)

Author Affiliations
From the Department of Surgery, Brown University (Drs Amaral, Gann, and Caldwell, and Messrs Shearer and Mastrofrancesco) and the Surgical Metabolism Laboratory, The Rhode Island Hospital (Messrs Shearer and Mastrofrancesco and Dr Caldwell), Providence, RI.

Footnotes
Accepted for publication March 15, 1988.

Reprint requests to Department of Surgery, The Rhode Island Hospital, 593 Eddy St, Providence, RI 02902 (Dr Caldwell).

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