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Articles in PresS, published online ahead of print March 5, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00545.2001
Submitted on December 7, 2001
Accepted on February 21, 2002
1 Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA; Mouse Metabolic Physiology Center, Vanderbilt University School of Medicine, Nashville, TN, USA; Pharmacology, Vanderbilt University School of Medicine, Nashville, TN, USA
2 Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN, USA; Mouse Metabolic Physiology Center, Vanderbilt University School of Medicine, Nashville, TN, USA
3 Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA
4 Radiology, Vanderbilt University School of Medicine, Nashville, TN, USA
* To whom correspondence should be addressed. E-mail: jeff.rottman{at}mcmail.vanderbilt.edu.
Isotopic techniques were used to test the hypothesis that exercise and nitric oxide synthase (NOS) inhibition have distinct effects on tissue-specific fatty acid and glucose uptakes in a conscious chronically catheterized mouse model. Uptakes were measured using the radioactive tracers [125I]beta-methyl-p-iodophenylpentadecanoic acid (BMIPP) and [2-3H]deoxyglucose (DG) during treadmill exercise, with and without inhibition of NOS. [125I]BMIPP uptake at rest differed substantially among tissues with the highest levels in heart. With exercise, [125I]BMIPP uptake increased in both heart and skeletal muscles. In sedentary mice NOS inhibition induced by L-NAME feeding increased heart and soleus [125I]BMIPP uptake. In contrast, exercise, but not L-NAME feeding, resulted in increased heart and skeletal muscle [2-3H]DG uptake. Significant interactions were not observed in the effects of combined exercise and L-NAME feeding on [125I]BMIPP and [2-3H]DG uptakes. In the conscious mouse exercise and NOS inhibition produce distinct patterns of tissue-specific fatty acid and glucose uptake; NOS is not required for important components of exercise-associated metabolic signaling, or other mechanisms compensate for the absence of this regulatory mechanism.
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