The principle finding of this study is
the further demonstration of the metabolic inflexibility
of skeletal muscle myotubes developed from
morbidly obese individuals. It was demonstrated
that the acute exposure of cultured skeletal muscle
myotubes derived from obese individuals to leptin
failed to alter the expression of several key
lipid oxidative and mitochondrial genes. Contrary
to the obese derived myotubes, cells derived from
lean and healthy controls demonstrated a capacity
to increase the expression of several key genes.
Further analysis is required to elucidate the mechanisms
involved, with studies needed to examine
leptin-receptor mediated events.