Ana Francisca Soares1,2, John Griffith Jones1, Francisco Veiga2, Rui Albuquerque Carvalho1
1Biochemistry and Center for Neurosciences and Cell Biology, University of Coimbra, Coimbra, Portugal; 2Pharmaceutical Technology, University of Coimbra, Coimbra, Portugal
Hepatic glycogen fluxes were characterized in 24-hour fasted rats following an oral tracer-enriched load. Combination of 13C isotopomer analysis with 2H-enrichment from 2H2O, resolved load contribution from that of endogenous gluconeogenesis to hepatic glycogen. The latter accounted for 66 13 % of the glycogen synthesized during the experiment whereas less than one third originated in the oral load following direct and indirect pathways at similar extents: 18 3 % and 16 2 %, respectively. Thus hepatic glycogen synthesis contributes to normoglygemia mostly by diverting gluconeogenic carbons from hepatic glucose production rather than through net uptake of glucose.