Absence of intestinal gluconeogenesis in rats and dogs

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We investigated the potential for intestinal gluconeogenesis in vivo by determining the arterio-venous balances of concentration and isotopic enrichment (IE) of [6,6-2H2]glucose across various organs. The gas chromatography-mass spectrometry data were integrated using a recently developed method that amplifies the apparent IE while improving the precision of the measurements. In 48 hr-fasted rats receiving a constant infusion of [6,6-2H2]glucose, we could not detect a difference in glucose IE across the intestine (n = 7, 4 pairs of samples per rat). To test whether deep hypoglycemia would induce intestinal glucose production, we studied acutely hepatectomized 48 hr-fasted dogs. When the liver was clamped, we injected a 1.1 mmol bolus of [6,6-2H2]glucose. Over the next 2 hr, arterial glucose concentration and IE decreased from ~ 5 mM to ~ 0.5 mM and from ~ 1.25% to ~ 0.25%, respectively (the later resulted from some glucose production in the kidney, demonstrated by a small detectable difference in glucose IE between arterial and renal vein plasma). However, the renal glucose production did not prevent deep hypoglycemia. In addition, there was no detectable difference in glucose IE or concentration between arterial and portal vein plasma (n = 5 dogs, 8 to 12 pairs of samples per dog). We conclude that there is no detectable intestinal gluconeogenesis in dogs and rats in vivo. Supported by NIH Roadmap grant 5 R33 DK070291.