Hepatic abnormalities have been noted in adults since the beginning of hyperalimentation. Which of the following statements are true?

A. Hepatic steatosis appears to be associated with an overload of glucose.

D. Abnormalities in the portal insulin-glucagon ratio are thought to be causative of hepatic steatosis in experimental animals

DISCUSSION: The most common metabolic complication of TPN in adults is hepatic steatosis. Unlike the hepatic abnormalities in children, which may progress to cholestasis, liver damage, and in some cases death, hepatic steatosis, or fatty infiltration of the liver with triglycerides, appears to be a rather benign complication. It may be, but is not necessarily, associated with hepatic enzymatic abnormalities, which usually occur in the first week, peak at the third week, and generally disappear by the sixth week of parenteral nutrition. Abnormalities in the transaminases are most common, with alkaline phosphatase also being elevated, but there is no correlation between the degree of fatty infiltration and enzymatic abnormalities. Fatty infiltration appears to be largely vacuolization with increased storage of triglycerides. Hepatic steatosis is almost always associated with an overload of glucose. Recent studies in experimental animals have suggested that the portal insulin-glucagon ratio, which is elevated under these circumstances, may be causally related to hepatic steatosis. Insulin is the leading storage enzyme and is responsible for lipogenesis. The presence of insulin inhibits lipolysis. Glucagon, on the other hand, results in the mobilization of hepatic lipid. The liver “sees” the portal vein insulin-glucagon ratio. Excesses of insulin elicited by hypertonic dextrose increase lipid deposition in the liver, whereas glucagon, which is elicited by certain amino acids, results in the mobilization of hepatic lipid.