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An in-line digestive cartridge increases enteral fat and vitamin absorption in a porcine model of short bowel syndrome.
Clin Nutr. 2022 05; 41(5):1093-1101.CN

Abstract

BACKGROUND & AIMS

Short bowel syndrome (SBS) occurs after intestinal loss resulting in parenteral nutrition dependence and micronutrient deficiencies, which may lead to life-limiting complications. ALC-078 is a cartridge containing immobilized lipase that connects in-line with enteral feeding sets and digests fats in enteral nutrition (EN). In this study, we evaluate the efficacy of ALC-078 to improve fat and nutrient absorption in a porcine SBS model.

METHODS

Fifteen male Yorkshire piglets were assessed. Animals were randomized to no intestinal resection (n = 5), 75% resection (n = 5), or 75% resection + ALC-078 (n = 5). After recovery, animals were treated for 14 days. Piglets received 60% of nutrition from continuous EN and 40% from chow. The degree of fat malabsorption was determined by the coefficient of fat absorption (CFA) following a 72-h stool collection. Body weight, fat-soluble vitamins, and nutritional markers were assessed.

RESULTS

Adverse events were similar across the three groups (P = 1.00). ALC-078-treated animals had similar weight gain compared to resected piglets. Resected animals had a lower CFA compared to unresected controls (79.3% vs. 95.2%, P = 0.01) while there was no significant difference in the ALC-078 animals (87.1% vs. 95.2%, P = 0.19). Between Study Days 1 and 15, ALC-078 animals had increased concentrations of vitamin D (12.2 vs. 8.7 ng/mL, P = 0.0006), and vitamin E (4.3 vs. 2.5 mg/L, P = 0.03). These markers did not significantly change in untreated resected animals.

CONCLUSION

ALC-078 increases the absorption of fat-soluble vitamins and may improve fat malabsorption. Future studies should determine whether ALC-078 can reduce PN dependence and if these findings translate to human patients with SBS.

Links

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Authors+Show Affiliations

Tsikis ST
Vascular Biology Program, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA; Department of Surgery, Boston Children's Hospital, Harvard Medical School, 300 Longwood Ave, Fegan 3, Boston, MA 02115, USA.
Fligor SC
Vascular Biology Program, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA; Department of Surgery, Boston Children's Hospital, Harvard Medical School, 300 Longwood Ave, Fegan 3, Boston, MA 02115, USA.
Secor JD
Vascular Biology Program, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA; Department of Surgery, Boston Children's Hospital, Harvard Medical School, 300 Longwood Ave, Fegan 3, Boston, MA 02115, USA.
Yu LJ
Vascular Biology Program, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA; Department of Surgery, Boston Children's Hospital, Harvard Medical School, 300 Longwood Ave, Fegan 3, Boston, MA 02115, USA.
Pan A
Vascular Biology Program, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA; Department of Surgery, Boston Children's Hospital, Harvard Medical School, 300 Longwood Ave, Fegan 3, Boston, MA 02115, USA.
Mitchell PD
Institutional Centers for Clinical and Translational Research, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA, 02115, USA.
Loring G
Alcresta Therapeutics, Newton, MA 02462, USA.
First E
Alcresta Therapeutics, Newton, MA 02462, USA.
Nedder AP
Animal Care Resources Children's Hospital, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA.
Grammer RM
Animal Care Resources Children's Hospital, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA.
Pattison B
Animal Care Resources Children's Hospital, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA.
Gura KM
Department of Pharmacy and the Division of Gastroenterology and Nutrition, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA.
Puder M
Vascular Biology Program, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA; Department of Surgery, Boston Children's Hospital, Harvard Medical School, 300 Longwood Ave, Fegan 3, Boston, MA 02115, USA. Electronic address: Mark.Puder@childrens.harvard.edu.

MeSH

AnimalsMaleDisease Models, AnimalEnteral NutritionIntestine, SmallParenteral NutritionShort Bowel SyndromeSwineVitamins

Pub Type(s)

Journal Article

Language

eng

PubMed ID

35413571

Citation

Tsikis, S T., et al. "An In-line Digestive Cartridge Increases Enteral Fat and Vitamin Absorption in a Porcine Model of Short Bowel Syndrome." Clinical Nutrition (Edinburgh, Scotland), vol. 41, no. 5, 2022, pp. 1093-1101.
Tsikis ST, Fligor SC, Secor JD, et al. An in-line digestive cartridge increases enteral fat and vitamin absorption in a porcine model of short bowel syndrome. Clin Nutr. 2022;41(5):1093-1101.
Tsikis, S. T., Fligor, S. C., Secor, J. D., Yu, L. J., Pan, A., Mitchell, P. D., Loring, G., First, E., Nedder, A. P., Grammer, R. M., Pattison, B., Gura, K. M., & Puder, M. (2022). An in-line digestive cartridge increases enteral fat and vitamin absorption in a porcine model of short bowel syndrome. Clinical Nutrition (Edinburgh, Scotland), 41(5), 1093-1101. https://doi.org/10.1016/j.clnu.2022.03.026
Tsikis ST, et al. An In-line Digestive Cartridge Increases Enteral Fat and Vitamin Absorption in a Porcine Model of Short Bowel Syndrome. Clin Nutr. 2022;41(5):1093-1101. PubMed PMID: 35413571.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - An in-line digestive cartridge increases enteral fat and vitamin absorption in a porcine model of short bowel syndrome. AU - Tsikis,S T, AU - Fligor,S C, AU - Secor,J D, AU - Yu,L J, AU - Pan,A, AU - Mitchell,P D, AU - Loring,G, AU - First,E, AU - Nedder,A P, AU - Grammer,R M, AU - Pattison,B, AU - Gura,K M, AU - Puder,M, Y1 - 2022/03/31/ PY - 2022/02/02/received PY - 2022/03/18/revised PY - 2022/03/21/accepted PY - 2022/4/13/pubmed PY - 2022/5/3/medline PY - 2022/4/12/entrez KW - Digestive cartridge KW - Immobilized lipase KW - Intestinal failure KW - Micronutrient deficiencies KW - Short bowel syndrome SP - 1093 EP - 1101 JF - Clinical nutrition (Edinburgh, Scotland) JO - Clin Nutr VL - 41 IS - 5 N2 - BACKGROUND & AIMS: Short bowel syndrome (SBS) occurs after intestinal loss resulting in parenteral nutrition dependence and micronutrient deficiencies, which may lead to life-limiting complications. ALC-078 is a cartridge containing immobilized lipase that connects in-line with enteral feeding sets and digests fats in enteral nutrition (EN). In this study, we evaluate the efficacy of ALC-078 to improve fat and nutrient absorption in a porcine SBS model. METHODS: Fifteen male Yorkshire piglets were assessed. Animals were randomized to no intestinal resection (n = 5), 75% resection (n = 5), or 75% resection + ALC-078 (n = 5). After recovery, animals were treated for 14 days. Piglets received 60% of nutrition from continuous EN and 40% from chow. The degree of fat malabsorption was determined by the coefficient of fat absorption (CFA) following a 72-h stool collection. Body weight, fat-soluble vitamins, and nutritional markers were assessed. RESULTS: Adverse events were similar across the three groups (P = 1.00). ALC-078-treated animals had similar weight gain compared to resected piglets. Resected animals had a lower CFA compared to unresected controls (79.3% vs. 95.2%, P = 0.01) while there was no significant difference in the ALC-078 animals (87.1% vs. 95.2%, P = 0.19). Between Study Days 1 and 15, ALC-078 animals had increased concentrations of vitamin D (12.2 vs. 8.7 ng/mL, P = 0.0006), and vitamin E (4.3 vs. 2.5 mg/L, P = 0.03). These markers did not significantly change in untreated resected animals. CONCLUSION: ALC-078 increases the absorption of fat-soluble vitamins and may improve fat malabsorption. Future studies should determine whether ALC-078 can reduce PN dependence and if these findings translate to human patients with SBS. SN - 1532-1983 UR - https://www.unboundmedicine.com/medline/citation/35413571/An_in_line_digestive_cartridge_increases_enteral_fat_and_vitamin_absorption_in_a_porcine_model_of_short_bowel_syndrome_ DB - PRIME DP - Unbound Medicine ER -