| Supplementation of total parenteral nutrition with butyrate acutely increases structural aspects of intestinal adaptation after an 80% jejunoileal resection in neonatal piglets. | |
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MedLine Citation:
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PMID: 15291402 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Supplementation of total parenteral nutrition (TPN) with a mixture of short-chain fatty acids (SCFA) enhances intestinal adaptation in the adult rodent model. However, the ability and timing of SCFA to augment adaptation in the neonatal intestine is unknown. Furthermore, the specific SCFA inducing the intestinotrophic effects and underlying regulatory mechanism(s) are unclear. Therefore, we examined the effect of SCFA supplemented TPN on structural aspects of intestinal adaptation and hypothesized that butyrate is the SCFA responsible for these effects. METHODS: Piglets (n = 120) were randomized to (1) control TPN or TPN supplemented with (2) 60 mmol/L SCFA (36 mmol/L acetate, 15 mmol/L propionate and 9 mmol/L butyrate), (3) 9 mmol/L butyrate, or (4) 60 mmol/L butyrate. Within each group, piglets were further randomized to examine acute (4, 12, or 24 hours) and chronic (3 or 7 days) adaptations. Indices of intestinal adaptation, including crypt-villus architecture, proliferation and apoptosis, and concentration of the intestinotrophic peptide, glucagon-like pepide-2 (GLP-2), were measured. RESULTS: Villus height was increased (p < .029) within 4 hours by supplemented TPN treatments. Supplemented TPN treatments increased (p < .037) proliferating cell nuclear antigen expression along the entire intestine. Indicative of an antiapoptotic profile, jejunal Bax:Bcl-w abundance was decreased (p = .033) by both butyrate-supplemented TPN treatments, and ileal abundance was decreased (p = .0002) by all supplemented TPN treatments, regardless of time. Supplemented TPN treatments increased (p = .016) plasma GLP-2 concentration at all time points. CONCLUSIONS: Butyrate is the SCFA responsible for augmenting structural aspects of intestinal adaptations by increasing proliferation and decreasing apoptosis within 4 hours postresection. The intestinotrophic mechanism(s) underlying butyrate's effects may involve GLP-2. Ultimately, butyrate administration may enable an infant with short-bowel syndrome to successfully transition to enteral feedings by maximizing their absorptive area. |
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Authors:
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Anne L Bartholome; David M Albin; David H Baker; Jens J Holst; Kelly A Tappenden |
Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: JPEN. Journal of parenteral and enteral nutrition Volume: 28 ISSN: 0148-6071 ISO Abbreviation: JPEN J Parenter Enteral Nutr Publication Date: 2004 Jul-Aug |
Date Detail:
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Created Date: 2004-08-04 Completed Date: 2005-03-24 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 7804134 Medline TA: JPEN J Parenter Enteral Nutr Country: United States |
Other Details:
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Languages: eng Pagination: 210-22; discussion 222-3 Citation Subset: IM |
Affiliation:
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Division of Nutritional Sciences, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adaptation, Physiological
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drug effects* Animals Animals, Newborn Apoptosis / drug effects Butyrates / administration & dosage, pharmacology* Cell Division / drug effects Disease Models, Animal Dose-Response Relationship, Drug Fatty Acids, Volatile / administration & dosage, pharmacology Glucagon-Like Peptide 2 Glucagon-Like Peptides Humans Ileum / metabolism, pathology, physiology, surgery Intestinal Absorption / drug effects Intestines / drug effects, physiology*, surgery Jejunum / metabolism, pathology, physiology, surgery Parenteral Nutrition, Total* Peptides / blood, metabolism* Random Allocation Short Bowel Syndrome / therapy* Swine |
| Grant Support | |
ID/Acronym/Agency:
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R01 DK 57682/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Butyrates; 0/Fatty Acids, Volatile; 0/Glucagon-Like Peptide 2; 0/Peptides; 62340-29-8/Glucagon-Like Peptides |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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