Ceramide accumulation has been implicated in the impairment of
insulin-stimulated
glucose transport in skeletal muscle following
saturated fatty acid (FA) exposure. Importantly, a single bout of exercise can protect against acute
lipid-induced
insulin resistance. The mechanism by which exercise protects against
lipid-induced
insulin resistance is not completely known but may occur through a redirection of FA toward
triacylglycerol (TAG) and away from
ceramide and
diacylglycerol (DAG). Therefore, in the current study, an in vitro preparation was used to examine whether a prior bout of exercise could confer protection against
palmitate-induced
insulin resistance and whether the pharmacological [50 μM
fumonisin B(1) (FB1)] inhibition of
ceramide synthesis in the presence of
palmitate could mimic the protective effect of exercise. Soleus muscle of sedentary (SED), exercised (EX), and SED in the presence of FB1 (SED+FB1) were incubated with or without 2 mM
palmitate for 4 h. This 2-mM
palmitate exposure impaired
insulin-stimulated
glucose transport (-28%, P < 0.01) and significantly increased
ceramide, DAG, and TAG accumulation in the SED group (P < 0.05). A single prior bout of exercise prevented the detrimental effects of
palmitate on
insulin signaling and caused a partial redistribution of FA toward TAG (P < 0.05). However, the net increase in
ceramide content in response to
palmitate exposure in the EX group was not different compared with SED, despite the maintenance of
insulin sensitivity. The incubation of soleus from SED rats with FB1 (SED+FB1) prevented the detrimental effects of
palmitate and caused a redirection of FA toward TAG accumulation (P < 0.05). Therefore, this research suggests that although inhibiting
ceramide accumulation can prevent the detrimental effects of
palmitate, a single prior bout of exercise appears to protect against
palmitate-induced
insulin resistance, which may be independent of changes in
ceramide content.