Carbohydrate dyshomeostasis is a characteristic feature of sepsis. Sep
sis elevates glucose uptake and cellular lactate levels in muscle. The
mechanisms responsible for these alterations are unknown. We examined
the effects of a chronic, intra-abdominal septic abscess upon glucose
uptake, the expression of the insulin receptor, glucose transporter p
roteins (Glut-1 and Glut-4) and mRNA, and the content of glycolytic in
termediates in muscle from the hindlimb. Sepsis caused a 67% increase
in glucose uptake compared with control. A differential expression of
the Glut-1 and Glut-4 transporter proteins in skeletal muscle of septi
c rats was observed. Sepsis increased the expression of Glut-1 protein
1.7-fold. The increased Glut-1 protein correlated with a similar incr
ease in the relative abundance of Glut-1 mRNA. In contrast, sepsis did
not alter the amount of Glut-4 protein and mRNA or insulin receptor p
rotein. The tissue content of glucose-6-phosphate was increased approx
imately twofold compared with control. The increase in the glucose-6-p
hosphate content was not associated with increased glycogen deposition
in skeletal muscle of septic animals. Analysis of the glycolytic inte
rmediates showed that only the lactate content of muscles from septic
rats was significantly elevated in sepsis. The results are consistent
with the hypothesis that sepsis enhances glucose uptake secondary to i
ncreased Glut-1 expression. Furthermore, once transported, glucose may
be preferentially metabolized to lactate.