Tissue-Specific Controls on Carbohydrate Catabolism during Anoxia in Goldfish

Abstract

Tissue-specific controls on carbohydrate metabolism regulate the response to anoxia in goldfish (Carassius auratus) and bring about the overall metabolic rate depression that is a key feature of anoxia tolerance. The effect of anoxia (24 h at 7 C under N2/ CO atmosphere) on glycogen phosphorylase activity and on the content of fructose2,6-bisphosphate was determined in eight tissues (liver, brain, kidney, gill, spleen, heart, and red and white skeletal muscle) of goldfish. Anoxia resulted in an increase in the percentage of phosphorylase in the active a form in brain but significantly reduced phosphorylase-a content in liver, kidney, spleen, and heart; total phosphorylase activity (a + b) was also reduced during anoxia in liver and gill. Levels of the phosphofructokinase activator, fructose-2,6-P2, dropped 10-fold in liver during anoxia and were also reduced in gill and spleen. Brain and heart showed the opposite response, a 3.5-fold rise in fructose-2,6-P2 during anoxia. The data support a relative decrease in glycolytic flux in tissues such as liver, spleen, gill, and kidney (in line with a general metabolic rate depression) and a relative increase in glycolysis in brain and heart. In liver, the sharp drop in fructose-2,6-P2 content is probably also important in directing glycogenolysis toward glucose export into the blood.