*Hepatic Lipid Homeostasis in NAFLD DOI: http://dx.doi.org/10.5772/intechopen.108168*

### **Figure 3.**

*A scheme of the lipophagy process. Lipophagy caused by nutrient deficiency can be divided into five main stages: (1) initiation, (2) nucleation, (3) extension, (4) fusion, and (5) degradation. The increase of cAMP/ATP ratio can activate AMPK, which inhibits mTORC1 and activates ULK1/2 through direct or indirect phosphorylation. The formed ULK1/2-ATG13-ATG101-focal adhesion kinase family interacting protein of 200 KD (FIP200) complex activates Beclin 1 and interacts with UVRAG, autophagy, and Beclin 1 regulator 1 (AMBRA1), VPS34 phosphoinositide-3-kinase regulatory subunit 4 (PI3KR4, such as VPS15) binds to form phosphatidylinositol 3-phosphate (PI3P) and connects with WD repeat protein interacting with phosphoinositides (WIPIs) to participate in the nucleation and elongation. In the elongation stage, ATG7 and ATG10 ligases connect ATG12 with ATG5 and combine with polyprotein ATG16 to form a complex by promoting ATG7 (E1) and ATG10 (E2). Pro-LC3-I is combined with phosphatidylethanolamine (PE) through ATG4, ATG7, and ATG3 to form LC3-II. LC3-II binds to the expanding autophagy membrane, recruits transporters such as P62/SQSTM1, and selects and wraps components such as cytoplasm or organelles in cells. Closed autophagosomes fuse with lysosomes to produce autophagy lysosomes, causing lumen acidification, hydrolase activation, and content degradation.*

using autophagosomes [52]. Studies have reported that the process of microlipophagy needs the core TG machinery [72, 73], while others demonstrate that microlipophagy does not require core TG proteins [74]. At present, there is insufficient research on the correlation between microlipophagy and NAFLD, and studies are needed to unveil its precise mechanism.
