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1 Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, USA
2 Department of Cardiology, Vanderbilt University, Nashville, TN, USA
3 Environmental & Civil Engineering, Vanderbilt University, Nashville, TN, USA
4 Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, USA; Diabetes Research and Training Center, Vanderbilt University, Nashville, TN, USA
* To whom correspondence should be addressed. E-mail: david.wasserman{at}vanderbilt.edu.
AMP-activated protein kinase (AMPK) independently increases glucose and long chain fatty acid (LCFA) utilization in isolated cardiac muscle preparations. Recent studies indicate this may be due AMPK-induced phosphorylation and activation of nitric oxide synthase (NOS). Given this, the aim of the present study was to assess the effects of AMPK stimulation by 5-aminoimidazole-4-carboxamide-1-B-D-ribofuranoside (AICAR, 10mg/kg/min) on glucose and LCFA utilization in cardiac muscle and to determine the NOS dependence of any observed effects. Catheters were chronically implanted in a carotid artery and jugular vein of Sprague-Dawley rats. Following 4d recovery, conscious, unrestrained rats were given either water, or water containing 1mg/ml nitro-L-arginine methylester (L-NAME) for 2.5d. After an overnight fast, rats underwent one of 4 protocols: saline, AICAR, AICAR+L-NAME, or AICAR+Intralipid (20%, 0.02ml/kg/min). Glucose was clamped at ~6.5mM in all groups, and an intravenous bolus of 2-deoxy[3H]glucose and [125I]-15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid was administered to obtain indices of glucose and LCFA uptake and clearance. Despite AMPK activation as evidenced by acetyl-CoA carboxylase (Ser221) and AMPK phosphorylation (Thr172), AICAR increased cardiac LCFA but not glucose clearance. L-NAME+AICAR established that this effect was not due to NOS activation while AICAR+Intralipid showed that increased cardiac LCFA clearance was not LCFA concentration dependent. These results demonstrate that in vivo, AMPK stimulation increases LCFA but not glucose clearance by a NOS independent mechanism.
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