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Spreading the Silence

knockout mice, which have defects in autophagy, the authors confirmed that the LD lipolysis in hepatocytes is autophagy dependent. Moreover, by EM analysis of wild-type mice, the authors describe three kinds of autophagosomes distinguished by their content: some contain only LDs, some contain both LDs and other cytoplasmic constituents, while others do not contain detectable LDs. Long starvation periods lead to an increase in LD-containing autophagosomes (lipophagosomes), highlighting the physiological significance of this process for survival. Furthermore, using high fat diet-fed mice, the authors suggest that autophagy is inhibited following excessive lipid consumption— aprocessthatmayhavemajortherapeutic implications. However, further experiments are needed to elucidate this process. In summary, lipophagy may act on the one hand as a homeostatic regulator that controls the size and number of LDs under basal conditions and on the other hand as a stress-induced survival mechanism that provides the cell with energy source (Figure 1). These exciting findings suggest that a novel type of autophagy (lipophagy) specifically regulates lipidhomeostasis.However,themolecular mechanism by which the autophagic machinery recognizes LDs is not clear. Several LD resident proteins regulate TGs degradation by cytosolic lipases and thus may play a role in the selectiverecruitment of the autophagic machinery. It remains unclear which lysosomal lipase(s) is responsible for TG breakdown. The identification of lipid-specific autophagy by Singh and colleagues (2009) raises new questions concerning the relationship between lipophagy and canonical autophagy as well as between lipophagy and cytosolic lipolysis. Thus, exploring whether cytosolic lipolysis also plays a role in LD clearance under starvation or in response to lipid load will greatly contribute to the understanding of this field of study. Similarly, it is also important to test whether the autophagic process contributes to what has been known as a cytosolic lipolysis, induced by stimuli such as chronic exposure of adipocytes to TNF and insulin. The regulation of the LD cycle of accumulation and degradation by lipophagy may also have great physiologicalconsequences,sinceanimpairedcycle could lead to disorders associated with obesity and type-2 diabetes (like fatty liver diseases). Therefore, deciphering the molecular mechanism governing this process may provide new therapeutic tools.