Conditions in which IHL accumulates

• Increased hepatic NEFA uptake due to higher fasting and/or postprandial plasma NEFA concentrations

• Low partition of fatty acids to skeletal muscle (low chylomicron clearance by muscle and low NEFA uptake)

• Elevated DNL; activated by elevated plasma glucose and insulin concentrations

• Limited capacity to increase hepatic VLDL–TAG secretion and hepatic mitochondrial oxidation