{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T15:19:16Z","timestamp":1790176756569,"version":"4.1.0"},"reference-count":30,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2002,1,25]],"date-time":"2002-01-25T00:00:00Z","timestamp":1011916800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["NMR in Biomedicine"],"published-print":{"date-parts":[[2002,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Acute liver failure was induced in rats by CCl<jats:sub>4<\/jats:sub> administration and its effects on the hepatic Krebs cycle and gluconeogenic fluxes were evaluated <jats:italic>in situ<\/jats:italic> by <jats:sup>13<\/jats:sup>C NMR isotopomer analysis of hepatic glucose following infusion of [U\u2010<jats:sup>13<\/jats:sup>C]propionate. In fed animals, CCl<jats:sub>4<\/jats:sub> injury caused a significant increase in relative gluconeogenic flux from 0.80\u2005\u00b1\u20050.10 to 1.34\u2005\u00b1\u20050.24 times the flux through citrate synthase (<jats:italic>p<\/jats:italic>\u2005&lt;\u20050.01). In 24\u2010h fasted animals, CCl<jats:sub>4<\/jats:sub>\u2010injury also significantly increased relative gluconeogenic flux from 1.36\u2005\u00b1\u20050.16 to 1.80\u2005\u00b1\u20050.22 times the flux through citrate synthase (<jats:italic>p<\/jats:italic>\u2005&lt;\u20050.01). Recycling of PEP via pyruvate and oxaloacetate was extensive under all conditions and was not significantly altered by CCl<jats:sub>4<\/jats:sub> injury. CCl<jats:sub>4<\/jats:sub> injury significantly reduced hepatic glucose output by 26% (42.8\u2005\u00b1\u20057.3 vs 58.1\u2005\u00b1\u20052.4\u2005\u00b5mol\/kg\/min, <jats:italic>p<\/jats:italic>\u2005=\u20050.005), which was attributed to a 26% decrease in absolute gluconeogenic flux from PEP (85.6\u2005\u00b1\u200514.6 vs 116\u2005\u00b1\u20054.8\u2005\u00b5mol\/kg\/min, <jats:italic>p<\/jats:italic>\u2005&lt;\u20050.01). These changes were accompanied by a 47% reduction in absolute citrate synthase flux (90.6\u2005\u00b1\u20058.0 to 47.6\u2005\u00b1\u20058.0\u2005\u00b5mol\/kg\/min, <jats:italic>p<\/jats:italic>\u2005&lt;\u20050.005), indicating that oxidative Krebs cycle flux was more susceptible to CCl<jats:sub>4<\/jats:sub> injury. The reduction in absolute fluxes indicate a significant loss of hepatic metabolic capacity, while the significant increases in relative gluconeogenic fluxes suggest a reorganization of metabolic activity towards preserving hepatic glucose output. 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