Fig. 2

Lipid metabolism in non-alcoholic fatty liver disease (NAFLD). a. Under physiological conditions, lipase breaks down triacylglycerol into monoacylglycerol and FFAs, which are then absorbed by intestinal epithelial enterocytes. Then, FFAs and monoacylglycerol are used to resynthesize triacylglycerol by two key enzymatic steps: the first by mannoside acetylglucosaminyltransferase (MGAT) and the second by diglyceride acyltransferase (DGAT). Triacylglycerols are incorporated into chylomicrons (CMs) and secreted into the lymphatic vessels. After catalyzed by lipase, the remnants of CMs absorbed by liver [68, 69]. b. Insulin promotes lipid storage by inhibiting lipolysis via adipose triglyceride lipase (ATGL), phosphodiesterase 3B (PDE3B) and protein kinase A (PKA)-controlled hormone-sensitive lipase (HSL) and perilipins (PLINs). However, in regard to insulin resistance conditions (such as obesity or type 2 diabetes mellitus [T2DM]), lower insulin sensitivity stimulates lipolysis, which then leads to more NEFA flux to the liver. c. Several key enzymes (such as acetyl-CoA carboxylase [ACC], fatty acid synthase [FAS], stearoyl-CoA desaturase [SCD1] and DGAT2) are involved in de novo lipogenesis in the liver [222]