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Am J Physiol Endocrinol Metab 275: E843-E852, 1998;
0193-1849/98 $5.00
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Vol. 275, Issue 5, E843-E852, November 1998

13C NMR measurements of human gluconeogenic fluxes after ingestion of [U-13C]propionate, phenylacetate, and acetaminophen

John G. Jones1, Michael A. Solomon2, A. Dean Sherry1,3, F. M. H. Jeffrey1, and Craig R. Malloy1,2

1 Department of Radiology, University of Texas Southwestern Medical Center, Dallas 75235; 2 Department of Internal Medicine, University of Texas Southwestern Medical Center and Department of Veterans Affairs Medical Center, Dallas 75216; and 3 Department of Chemistry, University of Dallas, Richardson, Texas 75083

Anaplerotic, pyruvate recycling, and gluconeogenic fluxes were measured by 13C isotopomer analysis of plasma glucose, urinary phenylacetylglutamine, and urinary glucuronide in normal, 24-h-fasted individuals after ingestion of [U-13C]propionate, phenylacetate, and acetaminophen. Plasma glucose isotopomer analysis reported a total anaplerotic flux of 5.92 ± 1.03 (SD) relative to citrate synthase. This was not significantly different from glucuronide and phenylacetylglutamine analyses (6.08 ± 1.16 and 7.14 ± 1.94, respectively). Estimates of pyruvate recycling from glucose and glucuronide isotopomer distributions were almost identical (3.55 ± 0.99 and 3.66 ± 1.11, respectively), whereas phenylacetylglutamine reported a significantly higher estimate (5.74 ± 2.13). As a consequence, net gluconeogenic flux reported by phenylacetylglutamine (1.41 ± 0.28) was significantly less than that reported by glucose (2.37 ± 0.64) and glucuronide (2.42 ± 0.76). This difference in fluxes detected by analysis of phenylacetylglutamine vs. hexose is likely due to compartmentation of hepatic metabolism of propionate. Net gluconeogenic flux estimates made by use of this stable isotope method are in good agreement with recent measurements in humans with [14C]propionate.

glucose; glucuronide; glutamine; isotopomers; nuclear magnetic resonance


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