Non-Alcoholic Fatty Liver Disease: The Bile Acid-Activated Farnesoid X Receptor as an Emerging Treatment Target

Figure 1

Hepatic triglyceride (TG) formation, acquisition, and removal. Fatty liver is a result of an imbalance between free fatty acids (FFAs), and TG input and FFA and TG output. FFA derives from peripheral tissue, endogenous synthesis or diet in form of chylomicrons. Carbohydrate intake increases glucose and insulin levels thereby promoting lipogenesis through the activation of transcription factors sterol regulatory element-binding protein 1c (SREBP) and carbohydrate responsive element-binding protein (ChREBP). Reducing the FFA burden include β-oxidation in mitochondria, storage as TG, or export as very low-density lipoprotein (VLDL).