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Am J Physiol Endocrinol Metab 274: E954-E961, 1998;
0193-1849/98 $5.00
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Vol. 274, Issue 5, E954-E961, May 1998

SPECIAL COMMUNICATION
Limitations in estimating gluconeogenesis and Cori cycling from mass isotopomer distributions using [U-13C6]glucose

Bernard R. Landau, John Wahren, Karin Ekberg, Stephen F. Previs, Dawei Yang, and Henri Brunengraber

Departments of Medicine, Biochemistry, and Nutrition, Case Western Reserve University, Cleveland, Ohio 44106-4951; and Division of Clinical Physiology, Karolinska Hospital, 171 76 Stockholm, Sweden

Tayek and Katz proposed calculating gluconeogenesis's contributions to glucose production and Cori cycling from mass isotopomer distributions in blood glucose and lactate during [U-13C6]glucose infusion [Tayek, J. A., and J. Katz. Am. J. Physiol. 272 (Endocrinol. Metab. 35): E476-E484, 1997]. However, isotopic exchange was not adequately differentiated from dilution, nor was condensation of labeled with unlabeled triose phosphates properly equated. We introduce and apply corrected equations to data from subjects fasted for 12 and 60 h. Impossibly low contributions of gluconeogenesis to glucose production at 60 h are obtained (23-41%). Distributions in overnight-fasted normal subjects calculate to only ~18%. Cori cycling estimates are ~10-15% after overnight fasting and 20% after 60 h of fasting. There are several possible reasons for the underestimates. The contribution of gluconeogenesis is underestimated because glucose production from glycerol and amino acids not metabolized via pyruvate is ascribed to glycogenolysis. Labeled oxaloacetate and alpha -ketoglutarate can exchange during equilibrium with circulating unlabeled aspartate, glutamate, and glutamine. Also, the assumption that isotopomer distributions in arterial lactate and hepatic pyruvate are the same may not be fulfilled.

lactate; alanine; CO2 fixation


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