The result shows that while palmitic acid suppresses autophagic flux, exendin-4 increases the flux even in the presence of palmitic acid. It should be noted that while exendin appears to be lowering the autophagic flux in comparison to control, the difference is not statistically significant. To confirm if the increase in autophagy related genes actually resulted in an increased number of autophagosomes and whether there was indeed more lipophagy, we examined samples by transmission electron microscopy . Total number of autophagosomes that had lipid droplets in them and the total number of autophagolysosomes with lipid droplets were measured. Together these bodies are taken as autophagic vacuoles . Exendin WY 14643 treatment increased the number of AVs, although the number of autophagosomes and ALs varied with treatment. In oleic acid treated hepatocytes there was an insignificant change in AVs after exendin treatment, although the autophagosome count was significantly increased by exendin-4. There was a clear increase in both autophagosomes and ALs under palmitic acid and exendin treatments . Elaidic acid treatment with or without exendin resulted in a similar number of autophagosomes, however, exedin-4 treatment significantly increased the number of ALs . While visualizing cells for AVs we observed that some large sized lipid droplets had ��shriveled�� margins with distinct absence of autophagic vacuoles around them . We hypothesized that this may be a result of change in contents of the lipid droplet, perhaps due to transport of fatty acids for beta oxidation. To confirm enhanced b-oxidation we determined the concentration of ketone bodies, the final breakdown product of beta oxidation. ? hydroxybutyrate served as a marker for oxidation.