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© 2001 by the American Diabetes Association, Inc.
Nitric Oxide Increases Glucose Uptake Through a Mechanism That Is Distinct From the Insulin and Contraction Pathways in Rat Skeletal Muscle
From the Research Division, Joslin Diabetes Center; Department of Medicine, Brigham and Women's Hospital; and Harvard Medical School, Boston, Massachusetts.
Address correspondence and reprint requests to Laurie J. Goodyear, PhD, Research Division, Joslin Diabetes Center, 1 Joslin Place, Boston, MA 02215. E-mail: laurie.goodyear{at}joslin.harvard.edu .
Insulin, contraction, and the nitric oxide (NO) donor, sodium nitroprusside
(SNP), all increase glucose transport in skeletal muscle. Some reports suggest
that NO is a critical mediator of insulin- and/or contraction-stimulated
transport. To determine if the mechanism leading to NO-stimulated glucose
uptake is similar to the insulin- or contraction-dependent signaling pathways,
isolated soleus and extensor digitorum longus (EDL) muscles from rats were
treated with various combinations of SNP (maximum 10 mmol/l), insulin (maximum
50 mU/ml), electrical stimulation to produce contractions (maximum 10 min),
wortmannin (100 nmol/l), and/or the NO synthase (NOS) inhibitor
NG-monomethyl-L-arginine (L-NMMA) (0.1 mmol/l). The
combinations of SNP plus insulin and SNP plus contraction both had fully
additive effects on 2-deoxyglucose uptake. Wortmannin completely inhibited
insulinstimulated glucose transport and only slightly inhibited SNP-stimulated
2-deoxyglucose uptake, whereas L-NMMA did not inhibit contraction-stimulated
2-deoxyglucose uptake. SNP significantly increased the activity of the
1 catalytic subunit of 5' AMP-activated protein kinase (AMPK), a
signaling molecule that has been implicated in mediating glucose transport in
fuel-depleted cells. Addition of the NOS inhibitor
NG-nitro-L-arginine methyl ester (L-NAME) (1 mg/ml) to the
drinking water of rats for 2 days failed to affect the increase in muscle
2-deoxyglucose uptake in response to treadmill exercise. These data suggest
that NO stimulates glucose uptake through a mechanism that is distinct from
both the insulin and contraction signaling pathways.
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