Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/82058
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Type: Journal article
Title: The effects of critical illness on intestinal glucose sensing, transporters and absorption
Author: Deane, A.
Rayner, C.
Keeshan, A.
Cvijanovic, N.
Marino, Z.
Nguyen, Q.
Chia, B.
Summers, M.
Sim, J.
van Beek, T.
Chapman, M.
Horowitz, M.
Young, R.
Citation: Critical Care Medicine, 2014; 42(1):57-65
Publisher: Lippincott Williams & Wilkins
Issue Date: 2014
ISSN: 0090-3493
1530-0293
Statement of
Responsibility: 
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, Richard L. Young
Abstract: Objectives: Providing 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. Design: Prospective observational study in humans and mice. Setting: ICU and university-affiliated research laboratory. Subjects: Human subjects were 12 critically ill patients and 12 healthy controls. In the laboratory 16-week-old mice were studied. Interventions: Human 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 Results: Quantitative 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 sodiumdependent 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). Conclusions: Critical 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.
Keywords: blood glucose; enteral nutrition; glucose absorption; intensive care; small intestine
Rights: Copyright: © 2014 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins
RMID: 0020134387
DOI: 10.1097/CCM.0b013e318298a8af
Appears in Collections:Anaesthesia and Intensive Care publications

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