title: Glucose absorption and small intestinal transit in critical illness.
abstract: OBJECTIVE
  Although enteral nutrition is standard care for critically ill patients, nutrient absorption has not been quantified in this group and may be impaired due to intestinal dysmotility. The objectives of this study were to measure small intestinal glucose absorption and duodenocecal transit and determine their relationship with glycemia in the critically ill.
  
  
  METHODS
  Prospective observational study of healthy and critically ill subjects.
  
  
  METHODS
  Tertiary mixed medical-surgical adult intensive care unit.
  
  
  METHODS
  Twenty-eight critically ill patients and 16 healthy subjects were studied. MATERIALS AND MAIN RESULTS: Liquid feed (100 kcal/100 mL), labeled with Tc-sulfur colloid and including 3 g of 3-O-methylglucose, was infused into the duodenum. Glucose absorption and duodenocecal transit were measured using the area under the 3-O-methylglucose concentration curve and scintigraphy, respectively. Data are median (range).
  
  
  CONCLUSIONS
  Glucose absorption was reduced in critical illness when compared to health (area under the concentration curve: 16 [1-32] vs. 20 [14-34] mmol/L·min; p = .03). Small intestinal transit times were comparable in patients and healthy subjects (192 [9-240] vs. 168 [6-240] min; p = .99) and were not related to glucose absorption. Despite higher fasting blood glucose concentrations (6.3 [5.1-9.3] vs. 5.7 [4.6-7.6] mmol/L; p < .05), the increment in blood glucose was sustained for longer in the critically ill (Δ glucose at t = 60; 1.9 [-2.1-5.0] mmol/L vs. -0.2 [-1.3-2.3] mmol/L; p < .01).
  
  
  CONCLUSIONS
  Critical illness is associated with reduced small intestinal glucose absorption, but despite this, the glycemic response to enteral nutrient is sustained for longer.
authors.affiliation: National Health and Medical Research Council of Australia Centre for Clinical Research Excellence in Nutritional Physiology and Outcomes, Adelaide, South Australia, Australia. Adam.Deane@adelaide.edu.au
authors.forename: Adam M
authors.initials: AM
authors.lastname: Deane
authors.forename: Matthew J
authors.initials: MJ
authors.lastname: Summers
authors.forename: Antony V
authors.initials: AV
authors.lastname: Zaknic
authors.forename: Marianne J
authors.initials: MJ
authors.lastname: Chapman
authors.forename: Anna E
authors.initials: AE
authors.lastname: Di Bartolomeo
authors.forename: Max
authors.initials: M
authors.lastname: Bellon
authors.forename: Anne
authors.initials: A
authors.lastname: Maddox
authors.forename: Antoinette
authors.initials: A
authors.lastname: Russo
authors.forename: Michael
authors.initials: M
authors.lastname: Horowitz
authors.forename: Robert J L
authors.initials: RJ
authors.lastname: Fraser
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016022:Case-Control Studies; D002432:Cecum / Q000502:physiology; D016638:Critical Illness; D004386:Duodenum / Q000502:physiology*; D004750:Enteral Nutrition; D005260:Female; D005772:Gastrointestinal Transit / Q000502:physiology*; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D006943:Hyperglycemia / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D007408:Intestinal Absorption / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D055815:Young Adult
chemical_list: D005947:Glucose