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https://hdl.handle.net/2142/84932
Description
Title
Nutrient Transport During Hypoperfusion
Author(s)
Kles, Keri A.
Issue Date
2002
Doctoral Committee Chair(s)
Kelly A. Tappenden
Department of Study
Nutritional Sciences
Discipline
Nutritional Sciences
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Biology, Animal Physiology
Language
eng
Abstract
Intestinal hypoperfusion compromises many biochemical and physiological functions, such as ion exchange, access to nutrients and energy production, and is believed to play a pathogenic role in both necrotizing enterocolitis (NEC) and nonocclusive small bowel necrosis (NOSBN). It is postulated that the detrimental effects of hypoperfusion are further compounded by the provision of enteral nutrients. The studies presented within this dissertation provide a better understanding of the effect of hypoperfusion on the cellular mechanisms regulating nutrient transport during the provision of monosaccharides and glutamine and treatments to decrease injury. The effects of intestinal hypoperfusion on nutrient transport were elucidated in a piglet model, a rodent model and an established in vitro model. These studies demonstrate a nutrient independent downregulation of the sodium glucose cotransporter (SGLT-1) during hypoperfusion. Data from this thesis indicate that SGLT-1 is posttranslationally modified during hypoperfusion. In vitro investigations determined that the mechanism underlying impaired SGLT-1 activity during hypoxia is neither lowered intracellular pH nor cellular ATP depression, thereby implicating another hypoxia-associated alteration. It is possible that nutrients and peptide hormones can be used to upregulate nutrient transport in the compromised state. The addition of butyrate in vitro and ex vivo caused an increase in SGLT-1 transporter activity. Therefore, a study was performed to test the luminal addition of butyrate and the exogenous addition of peptide hormones such as glucagon-like peptide-2 (GLP-2) to prevent the detrimental effects during NEC-injury. These results indicate that NEC-injury was created in the nutrient perfused loops by decreasing barrier function, increasing morphological injury, increasing inflammation and altering nutrient transport. These data indicate formula perfusion is a necessary component of NEC associated injury. Although the role of GLP-2 and butyrate during NEC-injury is inconclusive, this refined NEC-injury model allows further investigation into the role of GLP-2 and butyrate. Therefore, the data from these studies are useful to determine the role of nutrient transport during disease where hypoperfusion plays a role, such as NEC and NOSBN, thereby providing insight into the relevant formula composition.
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