| dc.description.abstract | 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 | en |
