While the molecular mechanism is largely unknown, autophagy contributes at least partially to the supply of free fatty acids in response to fasting (Figure 3(e) ). Fasting provokes the increase of the levels of free fatty acids circulating in the blood, which are mobilized from adipose tissues. These free fatty acids are rapidly captured by various organs including hepatocytes and then transformed into triglycerides by esterification within lipid droplets. These lipid droplets appear to be turned over by a selective type of autophagy that has been named lipophagy in order to provide endogenous free fatty acids for energy production through β-oxidation [148] . Indeed, liver-specific Atg7 deficient mice display massive accumulation of triglycerides and cholesterol in the form of lipid droplets [191] . Agoutirelated peptide-(AgRP-) expressing neurons also respond to increased circulating levels of free fatty acids after fasting and then induce autophagy to degrade the lipid droplets [192] . Similar to the case in hepatocytes, autophagy in the neurons supplies endogenous free fatty acids for energy production and seems to be necessary for gene expression of AgPR, which is a neuropeptide that increases appetite and decreases metabolism and energy expenditure [192] .