Suspended animation: the molecular basis of metabolic depression

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Abstract
An impressive array of organisms is capable of radically depressing basal metabolic rate and entering a hypometabolic state characterized by a marked reduction of many normal physiological functions. Environmental cues are often the trigger: low oxygen, low temperature, or lack of water, for example. Entry into a hypometabolic state does not, apparently, involve major biochemical reorganization but appears, instead, to result from molecular controls operating at a level "above" that of allosteric regulation of enzymes and "below" that of gene expression. The mechanisms involved are widely applicable to the coordinated inactivation of many cellular processes. Studies of anaerobiosis in marine molluscs provide the most complete information on the molecular mechanisms involved in metabolic rate depression. Glycolytic rate depression in the marine whelk involves (i) covalent modification of key regulatory enzymes (e.g., phosphofructokinase, pyruvate kinase) via enzyme phosphorylation to produce less active enzyme forms, (ii) dissociation of enzymes from complexes bound to the subcellular particulate fraction to disrupt pathway flux, and (iii) decreased levels of fructose-2,6-bisphosphate, a potent activator of phosphofructokinase, to help limit the anabolic uses of carbohydrate in the depressed state. Continuing studies are demonstrating the universality of these mechanisms as the basis of metabolic depression, including involvement in mammalian hibernation and anoxia tolerance in goldfish and turtles.

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