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A more recent version of this article appeared on January 1, 2007

Papers In Press, published online ahead of print October 24, 2006
J. Lipid Res., doi:10.1194/jlr.M600319-JLR200
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Submitted on July 20, 2006
Revised on September 28, 2006
Accepted on October 23, 2006

Metabolic flexibility is conserved in diabetic myotubes

Michael Gaster

KMEB, Dept. of Endochrinology, Odense University Hospital, Odense 5000

Corresponding Author: gaster{at}post7.tele.dk

The purpose of the present study was to test the hypothesis, that metabolic inflexibility is an intrinsic defect. Glucose and lipid oxidation were studied in human myotubes established from healthy lean and obese subjects and patients with type 2 diabetes (T2D). In lean myotubes, glucose oxidation is raised by increasing glucose concentrations (0-20 mmol/l) and acute insulin stimulation (p<0.05) while inhibited by palmitate (PA). PA oxidation is raised by increasing PA concentrations (0-0.6mmol/l), while 1.0 mmol/l PA inhibits its own oxidation (p<0.05). Furthermore, PA oxidation is increased by acute insulin stimulation (p<0.05) and inhibited by glucose. Already 0.05 mM PA and 2.5 mM glucose, significantly reduced glucose and PA oxidation (p<0.05) respectively. Glucose and PA oxidation were insulin sensitive in myotubes established from lean (46%, 17%, glucose and PA oxidation resp., p<0.05 vs basal), obese (31%, 14%, p<0.05), and T2D subjects (17%, 8%, p<0.05). PA supplementation both reduces basal and insulin-stimulated glucose oxidation by 33-44% (p<0.05) and myotubes were still insulin sensitive in all three groups (p<0.05). Taken together, the metabolic inflexibility described in obese and diabetic patients is not an intrinsic defect, but is rather based on an extra muscular mechanism i.e. inability to vary extra cellular fatty acid concentrations during insulin simulation. Thus, skeletal muscles are metabolic flexible per se.


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