pRecent reports have indicated that 48–72 h of fasting, Type 1 diabetes and high-protein feeding induce gluconeogenesis in the small intestine of adult rats iin vivo/i. 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 72 h-fasted adult rats were incubated with [3-sup13/supC]glutamine as substrate. After incubation, substrate utilization and product accumulation were measured by enzymatic and NMR spectroscopic methods. Although the segments utilized [sup13/supC]glutamine at high rates and accumulated sup13/supC-labelled products linearly for 30 min iin vitro/i, no substantial glucose synthesis could be detected. This was not due to the re-utilization of [sup13/supC]glucose initially synthesized from [sup13/supC]glutamine. Arteriovenous metabolite concentration difference measurements across the portal vein-drained viscera of 72 h-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 iin vivo/i. Therefore we challenge the view that the small intestine of the adult rat is a gluconeogenic organ./p
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