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Description:
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Heart -type fatty acid binding protein (H -FABP ) is a major fatty acid binding
factor in skeletal muscles . Genetic lack of H -FABP severely impairs the esterification
and oxidation of exogenous fatty acids in soleus muscles isolated from chow -fed mice
(CHOW -solei ) and high fat diet -fed mice (HFD -solei ) , and prevents the HFD -induced
accumulation of muscle triglycerides . Here , we examined the impact of H -FABP
deficiency on the relationship between fatty acid utilization and glucose oxidation .
Glucose oxidation was measured in isolated soleus muscles in the presence or absence of
1 mM palmitate (simple protocol ) or in the absence of fatty acid after preincubation with
1 mM palmitate (complex protocol ) . With the simple protocol , the mutation slightly
reduced glucose oxidation in CHOW -muscles , but markedly increased it in HFDmuscles ;
unexpectedly , this pattern was not altered by the addition of palmitate , which
reduced glucose oxidation in both CHOW - and HFD -solei irrespective of the mutation . In
the complex protocol , the mutation first inhibited the synthesis and accumulation of
triglycerides and then their mobilization ; with this protocol , the mutation increased
glucose oxidation in both CHOW - and HFD -solei . We conclude : (i ) H -FABP mediates a
non -acute inhibition of muscle glucose oxidation by fatty acids , likely by enabling both
the accumulation and mobilidoes not mediate the acute inhibitory effect of extracellular fatty acids on muscle glucose
oxidation ; (iii ) H -FABP affects muscle glucose oxidation in opposing ways , with
inhibition prevailing at high muscle triglyceride contents .zation of a critical mass of muscle triglycerides ; (ii ) H -FABP |