Glycogen storage disease type 0 glycogen primer. Its action is highly regulated by a mechanism of phosphorylation and dephosphorylation and modulated by counter-regulatory hormones including insulin, epinephrine, and glucagon. Mutations in the gene for liver glycogen synthetase (GYS2, 138571) result in decreased or absent activity of liver glycogen synthetase and moderately decreased amounts of structurally normal glycogen in the liver. Mutational studies of patients with glycogen-storage disease type 0 do not demonstrate correlations between genotype and phenotype. [3] A different gene (GYS1, 138570) encodes muscle glycogen synthetase, which has normal activity in patients with glycogen-storage disease type 0A. In the early stages of fasting, the
Cyclic ketogenic diet goals of a refeed are threefold: The refueled glycogen stores can then be used for higher-intensity training to maintain or increase endurance / muscle mass after the refeed. Normally this sort of training would be relatively impossible on a pure ketogenic diet, as glycogen stores in the body are almost constantly depleted. The refeed process can lead to gaining fat if more carbs are consumed than needed to replenish glycogen stores. The timing, duration, and macronutrient composition of a refeed are crucial to the overall success of the diet. According to a published article in the "British Journal of Nutriton"