Since AAs stimulate glucagon secretion, which should then increase hepatic AA catabolism, it has been hypothesized that hepatic resistance (associated with hepatic fat content) to glucagon's actions on AA metabolism leads to hyperglucagonemia and hyperglycemia.METHODSTo test this hypothesis, we therefore studied lean and obese individuals, the latter group with and without hepatic steatosis as defined by proton density fat fraction (PDFF) > 5%. The gene discussed is GCG; the disease is fatty liver disease.