{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/84937"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/84937","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Short-Chain Fatty Acids and Glucagon -Like Peptide-2 Enhance Intestinal Development and Adaptation","abstract":"In 2002, 43% of the ∼470,822 preterm infants were born at a low birth weight. These infants have a higher risk for intestinal dysfunctions indicating the use of total parenteral nutrition (TPN) to meet their nutritional needs. Despite its benefits, TPN is associated with many complications; hence, treatments aimed at minimizing the need for TPN are necessary. Glucagon-like peptide-2 (GLP-2) may be a therapeutic agent as it reduces TPN associated atrophy and increases enzyme and transporter activity. To examine this, we coinfused GLP-2 with TPN and found increased ileal mRNA and protein abundance of the brush border sodium-dependent glucose cotransporter, SGLT-1. However, the minimum effective dose that is necessary to enhance intestinal function is unknown. Therefore, GLP-2 was coinfused with TPN at three physiological doses: low, moderate and high. Results show that the mRNA abundance of the basolateral sodium-independent glucose transporter, GLUT2, was increased to enteral levels by all GLP-2 doses. Furthermore, the low GLP-2 dose increased brush border membrane (BBM) protein abundance of GLUT2. This increase corresponded with an increase in glucose uptake, indicating that GLP-2 may be enhancing neonatal intestinal function through the translocation of GLUT2 from the basolateral to the BBM. Systemic short-chain fatty acids and dietary fiber are reported to stimulate the secretion of GLP-2. Therefore, we supplemented TPN with butyrate and found increases in structural adaptation. The most marked effects were in the intestinal epithelium, with increased crypt-villus architecture resulting from increased proliferation and decreased apoptosis. Additionally, butyrate increased the plasma GLP-2 concentration through a rapid and specific increase in ileal and colonic mRNA abundance of proglucagon, the gene that encodes GLP-2. Thus, GLP-2 may mediate the intestinotrophic effects of butyrate. Further evidence for the intestinotrophic effects of GLP-2 was investigated using a degradation-resistant GLP-2 analog, teduglutide, in adult patients with short-bowel syndrome. Teduglutide increased crypt-villus architecture, glucose and glutamine transport and the protein expression of nutrient transporters. The provision of GLP-2 and supplementation of TPN with butyrate, which augments endogenous levels of GLP-2, may benefit patients with intestinal dysfunctions by maximizing their intestinal absorptive capacity, thereby enabling them to successfully transition to enteral feedings.","abstract_html":"In 2002, 43% of the ∼470,822 preterm infants were born at a low birth weight. These infants have a higher risk for intestinal dysfunctions indicating the use of total parenteral nutrition (TPN) to meet their nutritional needs. Despite its benefits, TPN is associated with many complications; hence, treatments aimed at minimizing the need for TPN are necessary. Glucagon-like peptide-2 (GLP-2) may be a therapeutic agent as it reduces TPN associated atrophy and increases enzyme and transporter activity. To examine this, we coinfused GLP-2 with TPN and found increased ileal mRNA and protein abundance of the brush border sodium-dependent glucose cotransporter, SGLT-1. However, the minimum effective dose that is necessary to enhance intestinal function is unknown. Therefore, GLP-2 was coinfused with TPN at three physiological doses: low, moderate and high. Results show that the mRNA abundance of the basolateral sodium-independent glucose transporter, GLUT2, was increased to enteral levels by all GLP-2 doses. Furthermore, the low GLP-2 dose increased brush border membrane (BBM) protein abundance of GLUT2. This increase corresponded with an increase in glucose uptake, indicating that GLP-2 may be enhancing neonatal intestinal function through the translocation of GLUT2 from the basolateral to the BBM. Systemic short-chain fatty acids and dietary fiber are reported to stimulate the secretion of GLP-2. Therefore, we supplemented TPN with butyrate and found increases in structural adaptation. The most marked effects were in the intestinal epithelium, with increased crypt-villus architecture resulting from increased proliferation and decreased apoptosis. Additionally, butyrate increased the plasma GLP-2 concentration through a rapid and specific increase in ileal and colonic mRNA abundance of proglucagon, the gene that encodes GLP-2. Thus, GLP-2 may mediate the intestinotrophic effects of butyrate. Further evidence for the intestinotrophic effects of GLP-2 was investigated using a degradation-resistant GLP-2 analog, teduglutide, in adult patients with short-bowel syndrome. Teduglutide increased crypt-villus architecture, glucose and glutamine transport and the protein expression of nutrient transporters. The provision of GLP-2 and supplementation of TPN with butyrate, which augments endogenous levels of GLP-2, may benefit patients with intestinal dysfunctions by maximizing their intestinal absorptive capacity, thereby enabling them to successfully transition to enteral feedings.","abstract_has_math":false,"creators":["Bartholome, Anne Louise"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Nutritional Sciences","degree_department":null,"school":null,"contributors":["Kelly A. Tappenden"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-09-25T22:31:03Z","date_published":"2015-09-25T22:31:03Z","updated_at":"2026-07-22T22:26:24Z","subjects":["Health Sciences, Human Development"],"languages":["eng"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["(MiAaPQ)AAI3153243"],"render_values":[{"text":"(MiAaPQ)AAI3153243","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/84937","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Kelly A. 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These infants have a higher risk for intestinal dysfunctions indicating the use of total parenteral nutrition (TPN) to meet their nutritional needs. Despite its benefits, TPN is associated with many complications; hence, treatments aimed at minimizing the need for TPN are necessary. Glucagon-like peptide-2 (GLP-2) may be a therapeutic agent as it reduces TPN associated atrophy and increases enzyme and transporter activity. To examine this, we coinfused GLP-2 with TPN and found increased ileal mRNA and protein abundance of the brush border sodium-dependent glucose cotransporter, SGLT-1. However, the minimum effective dose that is necessary to enhance intestinal function is unknown. Therefore, GLP-2 was coinfused with TPN at three physiological doses: low, moderate and high. Results show that the mRNA abundance of the basolateral sodium-independent glucose transporter, GLUT2, was increased to enteral levels by all GLP-2 doses. Furthermore, the low GLP-2 dose increased brush border membrane (BBM) protein abundance of GLUT2. This increase corresponded with an increase in glucose uptake, indicating that GLP-2 may be enhancing neonatal intestinal function through the translocation of GLUT2 from the basolateral to the BBM. Systemic short-chain fatty acids and dietary fiber are reported to stimulate the secretion of GLP-2. Therefore, we supplemented TPN with butyrate and found increases in structural adaptation. The most marked effects were in the intestinal epithelium, with increased crypt-villus architecture resulting from increased proliferation and decreased apoptosis. Additionally, butyrate increased the plasma GLP-2 concentration through a rapid and specific increase in ileal and colonic mRNA abundance of proglucagon, the gene that encodes GLP-2. Thus, GLP-2 may mediate the intestinotrophic effects of butyrate. Further evidence for the intestinotrophic effects of GLP-2 was investigated using a degradation-resistant GLP-2 analog, teduglutide, in adult patients with short-bowel syndrome. Teduglutide increased crypt-villus architecture, glucose and glutamine transport and the protein expression of nutrient transporters. The provision of GLP-2 and supplementation of TPN with butyrate, which augments endogenous levels of GLP-2, may benefit patients with intestinal dysfunctions by maximizing their intestinal absorptive capacity, thereby enabling them to successfully transition to enteral feedings.","Made available in DSpace on 2015-09-25T22:31:03Z (GMT). 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These infants have a higher risk for intestinal dysfunctions indicating the use of total parenteral nutrition (TPN) to meet their nutritional needs. Despite its benefits, TPN is associated with many complications; hence, treatments aimed at minimizing the need for TPN are necessary. Glucagon-like peptide-2 (GLP-2) may be a therapeutic agent as it reduces TPN associated atrophy and increases enzyme and transporter activity. To examine this, we coinfused GLP-2 with TPN and found increased ileal mRNA and protein abundance of the brush border sodium-dependent glucose cotransporter, SGLT-1. However, the minimum effective dose that is necessary to enhance intestinal function is unknown. Therefore, GLP-2 was coinfused with TPN at three physiological doses: low, moderate and high. Results show that the mRNA abundance of the basolateral sodium-independent glucose transporter, GLUT2, was increased to enteral levels by all GLP-2 doses. Furthermore, the low GLP-2 dose increased brush border membrane (BBM) protein abundance of GLUT2. This increase corresponded with an increase in glucose uptake, indicating that GLP-2 may be enhancing neonatal intestinal function through the translocation of GLUT2 from the basolateral to the BBM. Systemic short-chain fatty acids and dietary fiber are reported to stimulate the secretion of GLP-2. Therefore, we supplemented TPN with butyrate and found increases in structural adaptation. The most marked effects were in the intestinal epithelium, with increased crypt-villus architecture resulting from increased proliferation and decreased apoptosis. Additionally, butyrate increased the plasma GLP-2 concentration through a rapid and specific increase in ileal and colonic mRNA abundance of proglucagon, the gene that encodes GLP-2. Thus, GLP-2 may mediate the intestinotrophic effects of butyrate. Further evidence for the intestinotrophic effects of GLP-2 was investigated using a degradation-resistant GLP-2 analog, teduglutide, in adult patients with short-bowel syndrome. Teduglutide increased crypt-villus architecture, glucose and glutamine transport and the protein expression of nutrient transporters. The provision of GLP-2 and supplementation of TPN with butyrate, which augments endogenous levels of GLP-2, may benefit patients with intestinal dysfunctions by maximizing their intestinal absorptive capacity, thereby enabling them to successfully transition to enteral feedings.","Made available in DSpace on 2015-09-25T22:31:03Z (GMT). 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