Adaptation of Mitochondrial Metabolism in Liver Cirrhosis: Different Strategies to Maintain a Vital Function

Abstract

Mitochondrial function and structure in cirrhotic livers from humans or rats show a variety of changes as compared to control livers. Mitochondrial ATP production is reduced in rats with CC1₄- or thioacetamide-induced liver cirrhosis and in rats with secondary biliary cirrhosis. Activity of the electron transport chain is decreased in rats with secondary biliary cirrhosis. In rats with CCl₄-induced cirrhosis, the mitochondrial content of certain constituents of the respiratory chain (cytochrome a + a₃, cytochrome b and ubiquinone) is increased and activities of cytochrome c oxidase and ATPase are elevated. Similarly, in humans with liver cirrhosis, mitochondrial cytochrome a + a, content is elevated and has been used to assess the risk for hepatectomy. In rats with secondary biliary cirrhosis, compensatory strategies include increased mitochondrial volume per hepatocyte and possibly increased extramitochondrial ATP production (increased glycolysis). Thus, a variety of adaptive mechanisms are used to maintain mitochondrial function in cirrhotic livers.

Key Words:

• Biliary cirrhosis
• carbon tetrachloride
• humans
• liver cirrhosis
• metabolism
• mitochondria
• morphology
• rats
• thioacetamide