Altered hepatic and intestinal homeostasis in a neonatal murine model of short-term total parenteral nutrition and antibiotics

Author:

Mims Tahliyah S.1,Kumari Roshan2,Leathem Cameron1,Antunes Karen1,Joseph Sydney3,Yen Mei-I1,Ferstl Danielle1,Jamieson Sophia M.1,Sabbar Austin1,Biebel Claudia1,Lazarevic Nikolai1,Willis Nathaniel B.1,Henry Lydia2,Yen Chi-Liang E.1ORCID,Smith Joseph P.4,Gosain Ankush5,Meisel Marlies6,Willis Kent A.7ORCID,Talati Ajay J.2ORCID,Elabiad Mohammad. T.2,Hibl Brianne8,Pierre Joseph F.19ORCID

Affiliation:

1. Department of Nutritional Sciences, College of Agriculture and Life Science, University of Wisconsin-Madison, Madison, Wisconsin, United States

2. Department of Pediatrics, College of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee, United States

3. Department of Medicine, College of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee, United States

4. Department of Pharmacy, University of Wisconsin Hospitals and Clinics, Madison, Wisconsin, United States

5. Department of Pediatric Surgery, Children’s Hospital of Colorado, Denver, Colorado, United States

6. Department of Immunology, University of Pittsburg, Pittsburg, Pennsylvania, United States

7. Division of Neonatology, Department of Pediatrics, Heersink School of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama, United States

8. Department of Comparative Medicine, University of Tennessee Health Science Center, Memphis, Tennessee, United States

9. Department of Surgery, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, Wisconsin, United States

Abstract

This study successfully established a translationally relevant, murine neonatal parenteral nutrition (PN) model. Short-term PN is sufficient to induce hepatitis-associated cholestasis in a neonatal murine model that can be used to understand disease in early life. The administration of antibiotics during PN protects animals from bacterial translocation and proinflammatory responses but induces unique metabolic shifts that may predispose the liver toward early steatosis.

Funder

HHS | NIH | NCI | Basic Research Laboratory

HHS | NIH | NIAID | Division of Microbiology and Infectious Diseases, National Institute of Allergy and Infectious Diseases

HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases

HHS | NIH | National Heart, Lung, and Blood Institute

HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases

Publisher

American Physiological Society

Subject

Physiology (medical),Gastroenterology,Hepatology,Physiology

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