Figure 2. Metabolic flux of exogenous (glucose) and endogenous (glycogen) carbohydrate contributing to anaplerosis.

A, glucose is assimilated into the cell (glucose uptake: a) and then undergoes glycolysis (b) or glycogen synthesis (glycogenesis: c). Glycogen undergoes glycogenolysis (d) and subsequent glycolysis (b′). The resulting pyruvate can undergo oxidative decarboxylation (e from glucose; e′ from glycogen), resulting in cataplerotic (2C) acetyl‐CoA, or anaplerosis (f ′ from glycogen). Also shown is (cataplerotic) β‐hydroxybutyrate (βHB) utilisation (g), and total oxidation (h). B, assuming no other metabolic fates, glycogenolytic flux (d) is identical to glycogen‐derived glycolysis (b′), which is also the sum of pyruvate oxidation (e′) and anaplerosis (f ′). If oxidation of glycogen‐derived pyruvate is negligible (e.g. when abundant exogenous substrate, such as glucose and βHB, is available) then glycogenolysis (d) will equal anaplerosis (f ′). If alternative anaplerotic sources are available (e.g. exogenous glucose) then anaplerosis from glycogen will be low – basal f ′ (f ′_B); however, if glycogen is the sole anaplerotic resource, increased anaplerosis from glycogen will result: the additional anaplerosis from glycogen to facilitate βHB oxidation is designated f ′_KB. For further details see text.