Abstract
The mode of action of α-adrenergic agents and vasopressin on the regulation of gluconeogenesis is functionally related to a cellular Ca 2+ redistribution, but the mechanism or site of action of Ca 2+ in the gluconeogenic pathway is not agreed upon. In glycogenolysis, the role of Ca 2+ is pinpointed to phosphorylase kinase by calmodulin, the ubiquitous Ca 2+-binding protein, being part of the enzyme; the gluconeogenic pathway does not offer such a cue. This article presents a hypothesis on the role of Ca 2+ redistribution in the regulation of gluconeogenesis.
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