• Adam M Deane, Chris K Rayner, Alex Keeshan, Nada Cvijanovic, Zelia Marino, Nam Q Nguyen, Bridgette Chia, Matthew J Summers, Jennifer A Sim, Theresia van Beek, Marianne J Chapman, Michael Horowitz, and Richard L Young.
• 1Discipline of Acute Care Medicine, University of Adelaide, North Terrace, Adelaide, South Australia, Australia. 2Intensive Care Unit, Royal Adelaide Hospital, Adelaide, South Australia, Australia. 3Discipline of Medicine, University of Adelaide, Royal Adelaide Hospital, Adelaide, South Australia, Australia. 4Department of Gastroenterology and Hepatology, Royal Adelaide Hospital, Adelaide, South Australia, Australia. 5Discipline of Medicine, Nerve-Gut Research Laboratory, Level-1 Hanson Institute, Adelaide, South Australia, Australia.
• Crit. Care Med.. 2014 Jan 1;42(1):57-65.

ObjectivesProviding effective enteral nutrition is important during critical illness. In health, glucose is absorbed from the small intestine via sodium-dependent glucose transporter-1 and glucose transporter-2, which may both be regulated by intestinal sweet taste receptors. We evaluated the effect of critical illness on glucose absorption and expression of intestinal sodium-dependent glucose transporter-1, glucose transporter-2, and sweet taste receptors in humans and mice.DesignProspective observational study in humans and mice.SettingICU and university-affiliated research laboratory.SubjectsHuman subjects were 12 critically ill patients and 12 healthy controls. In the laboratory 16-week-old mice were studied.InterventionsHuman subjects underwent endoscopy. Glucose (30 g) and 3-O-methylglucose (3 g), used to estimate glucose absorption, were infused intraduodenally over 30 minutes. Duodenal mucosa was biopsied before and after infusion. Mice were randomized to cecal ligation and puncture to model critical illness (n = 16) or sham laparotomy (control) (n = 8). At day 5, mice received glucose (100 mg) and 3-O-methylglucose (10 mg) infused intraduodenally prior to mucosal tissue collection.Measurements And Main ResultsQuantitative polymerase chain reaction was performed to measure absolute (human) and relative levels of sodium-dependent glucose transporter-1, glucose transporter-2, and taste receptor type 1 member 2 (T1R2) transcripts. Blood samples were assayed for 3-O-methylglucose to estimate glucose absorption. Glucose absorption was three-fold lower in critically ill humans than in controls (p = 0.002) and reduced by a similar proportion in cecal ligation and puncture mice (p = 0.004). In critically ill patients, duodenal levels of sodium-dependent glucose transporter-1, glucose transporter-2, and T1R2 transcript were reduced 49% (p < 0.001), 50% (p = 0.009), and 85% (p = 0.007), whereas in the jejunum of cecal ligation and puncture mice sodium-dependent glucose transporter-1, glucose transporter-2, and T1R2 transcripts were reduced by 55% (p < 0.001), 50% (p = 0.002), and 69% (p = 0.004).ConclusionsCritical illness is characterized by markedly diminished glucose absorption, associated with reduced intestinal expression of glucose transporters (sodium-dependent glucose transporter-1 and glucose transporter-2) and sweet taste receptor transcripts. These changes are paralleled in cecal ligation and puncture mice.

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