Table 1.

The role of G protein-coupled receptors in nonalcoholic fatty liver disease, nonalcoholic steatohepatitis, and hepatocellular carcinoma

Liver disease	GPCRs	Expression	Ref.
NAFLD/Steatosis	GPR120	GPR120 agonist cpdA treatment increased insulin sensitivity and glucose tolerance and decreased hepatic steatosis in HFD-induced obese mice	[46]
HCC	GPR49	GPR49 is highly expressed in human HCC cell lines PLC/PRF/5 and HepG2; overexpression of GPR49 in HCC tissue with a mutation of beta-catenin exon 3 was also shown	[47]
HCC	GPR137	Knockdown of GPR137 in HepG2 cells induced cell cycle arrest and cell apoptosis. Additionally, low expression of GPR137 indicated the progression of human HCC and a low survival rate	[49]
NAFLD/Steatosis	GPR132	GPR132 was involved in hepatic lipid metabolism and gallstone formation in mice because GPR132-deficient mice fed a lithogenic diet quickly developed gallstones and had a high cholesterol saturation index	[51]
NAFLD/Steatosis	GPR55	GPR55-deficient (GPR55-/-) mice showed impaired insulin signaling and had a significant increase in total body fat and liver fatty acid synthase, resulting in the development of hepatic steatosis	[53]
NASH/Fibrosis	GPR91	Succinate in the fatty liver can activate HSC via GPR91 receptor, resulting in NASH progression	[45]
Liver injury/Fibrosis	GPBAR1	GPBAR1 is an upstream regulator of the axis expression of chemokine CCL2 and its receptor CCR2 in the interface of liver sinusoidal cells	[54]

GPCRs: G protein-coupled receptors; HCC: Hepatocellular carcinoma; HFD: High-fat diet; HSC: Hepatic stellate cell; NAFLD: Nonalcoholic fatty liver disease; NASH: Nonalcoholic steatohepatitis.