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Absence of intestinal gluconeogenesis in type 1 diabetic rats: carbon 13 NMR and arteriovenous concentration difference measurements

Recent reports have indicated that 48–72h of fasting, type 1 diabetes and high‐protein feeding induce gluconeogenesis in the small intestine of adult rats in vivo. Since this would (i) represent a dramatic revision of the prevailing view that only the liver and the kidneys are gluconeogenic, and (ii) have major consequences in the metabolism, nutrition and diabetes fields, we have thoroughly re‐examined this question in the situation reported to induce the highest rate of gluconeogenesis. For this, metabolically viable small intestinal segments from 72h‐fasted adult rats were incubated with [3‐13C]glutamine as substrate. After incubation, substrate utilization and product accumulation were measured by enzymatic and NMR methods. Although the segments utilized 13C‐glutamine at high rates and accumulated 13C‐labeled products linearly for 30 min in vitro, no substantial glucose synthesis could be detected. This was not due to the re‐utilization of 13C‐glucose initially synthesized. Arteriovenous metabolite concentration difference measurements across the portal vein‐drained viscera of 72h‐fasted Wistar and Sprague‐Dawley rats clearly indicated that glutamine, the main if not the only gluconeogenic precursor taken up, could not give rise to detectable glucose production in vivo. Therefore, we challenge the view that the small intestine of the adult rat is a gluconeogenic organ.