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Enteral nutrients alter enterocyte function within an in vitro model similar to an acute in vivo rat model during hypoxia
Author(s) -
Kles KA,
Turner JR,
Tappenden KA
Publication year - 2002
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1177/014860710202600271
Subject(s) - enterocyte , in vivo , hypoxia (environmental) , glutamine , enteral administration , medicine , adenosine , barrier function , endocrinology , pharmacology , glucose transporter , perfusion , biology , parenteral nutrition , biochemistry , chemistry , small intestine , insulin , oxygen , microbiology and biotechnology , organic chemistry , amino acid
BACKGROUND: Early enteral nutrition in patients following traumatic injury is an important intervention. However, after shock‐resuscitation, intestinal hypoperfusion persists despite adequate systemic resuscitation. Our previous in vivo rat studies indicate that hypoperfusion impairs mucosal function in the small intestine. Therefore, the current study sought to improve previous in vitro models by the following means: (1) We used Caco‐2 monolayers stably transfected with the brush‐border sodium‐glucose co‐transporter (SGLT‐1); and (2) we created an environment that mimicked the physiologic enterocyte environment. We hypothesized that hypoxic alterations of epithelial function in an in vitro model are comparable to those of an in vivo rat model. METHODS: After 21 days, monolayers were randomized to receive 24 hours of incubation in a normoxic or hypoxic environment. Cells were further randomized to receive 1 of 4 nutrient treatments: mannitol (an osmotic control), glucose (uses SGLT‐1 and is metabolized), 3‐O‐methylglucose (3‐O‐mg; uses SGLT‐1 and is not metabolized), or fructose (does not use SGLT‐1 but can be metabolized). RESULTS: Transepithelial resistance (p =.007) and short‐circuit current (p =.05) were lower in hypoxic groups. When compared with normoxic groups, hypoxic groups had significantly impaired glucose (p <.001) but not glutamine transport, irrespective of nutrient treatment. Additionally, adenosine triphosphate/adenosine diphosphate ratio was reduced (p =.01) and lactate concentration was increased (p <.001) during hypoxia. CONCLUSIONS: In summary, results from this in vitro study using Caco‐2BBe cells stably transfected with SGLT‐1 correspond to results obtained in the in vivo rat model. Therefore, this is an appropriate in vitro model in which to study cellular alterations caused by the hypoxic small intestine, with the goal of ensuring safe early enteral nutrition following traumatic injury.