Table 1. Reported Mechanisms for an Improvement of Liver Function due to SGLT2is.

SGLT2is	References	Subjects	Effects on liver and putative mechanisms to improve liver function
Ipragliflozin	[5]	Type 2 diabetic mice	Improvement of hepatic steatosis and liver injury; reduction of plasma and liver levels of oxidative stress biomarkers and inflammatory markers
Ipragliflozin	[6]	Type 1 diabetic rats	Improvement of hepatic steatosis and liver injury; reduction of liver levels of oxidative stress biomarkers and plasma levels of inflammatory markers
Ipragliflozin	[7]	NAFLD rats	Prevention of hepatic triglyceride accumulation, large lipid droplet formation and liver fibrosis
Ipragliflozin	[8]	Obese mice	Prevention of ectopic fat accumulation in the liver
Luseogliflozin	[9, 10]	Type 2 diabetic patients with NAFLD	Reduction of hepatic fat content
Empagliflozin	[11]	Well-controlled type 2 diabetic patients	Lowering of liver fat content
Canagliflozin	[12]	HEK-293 cells	AMPK activation by inhibition of Complex I of the respiratory chain; inhibition of lipid synthesis, by phosphorylation of ACC at the AMPK sites in human hepatocytes, which leads to downregulation of fatty acid synthesis-related molecules and upregulation of β oxidation-associated molecules
Tofogliflozin	[13]	C57BL/6 mice	Decrease of hepatic triglyceride content; acceleration of lipolysis in adipose tissue and hepatic β-oxidation

SGLT2is: sodium-glucose cotransporter-2 inhibitors; ACC: acetyl-CoA carboxylase; AMPK: adenosine 5'-monophosphate-activated protein kinase; NAFLD: nonalcoholic fatty liver disease; HEK: human embryonic kidney.