We determined whether habitual cigarette smoking alters insulin-stimulated
glucose transport and GLUT4 protein expression in skeletal muscle. Vastus l
ateralis muscle was obtained from 10 habitual cigarette smokers and 10 cont
rol subjects using an open muscle biopsy procedure. Basal 3-O-methylglucose
transport was twofold higher (P>0.01) in muscle from habitual smokers (0.0
5 +/- 0.08 vs. 1.04 +/- 0.19 mu mol ml(-1) h(-1); controls vs, smokers resp
ectively). Insulin (600 pmol l(-1)) increased glucose transport 2.6-fold (P
> 0.05) in muscle from control subjects, whereas no significant increase w
as noted in habitual smokers. Skeletal muscle GLUT4 protein expression was
similar between the groups. FFA levels were elevated in the smokers (264 +/
- 49 vs. 748 +/- 138 mu mol l(-1) for control subjects vs. smokers; P < 0.0
5), and serum triglyceride levels were increased in the smokers (0.9 +/- 0.
2 vs. 2.3 +/- 0.6 mmol l(-1) for control subjects vs. smokers; P < 0.05). S
keletal muscle carnitine palmitil (acyl) transferase activity was similar b
etween the groups, indicating that FFA transport into the mitochondria was
unaltered by cigarette smoking. In conclusion, cigarette smoking appears to
have a profound effect On glucose transport in skeletal muscle. Basal gluc
ose transport is markedly elevated, whereas insulin-stimulated glucose tran
sport is impaired. These changes cannot be explained by altered protein exp
ression of GLUT4, but may be related to increased serum FFA and triglycerid
e levels. These findings highlight the importance of identifying habitual c
igarette smokers in studies aimed at assessing factors that lead to alterat
ions in lipid and glucose homeostasis in people with non-insulin-dependent
diabetes mellitus (NIDDM).