Diet, Gut Microbiome, and Their End Metabolites Associate With Acute Pancreatitis Risk.


Journal

Clinical and translational gastroenterology
ISSN: 2155-384X
Titre abrégé: Clin Transl Gastroenterol
Pays: United States
ID NLM: 101532142

Informations de publication

Date de publication:
01 07 2023
Historique:
received: 02 11 2022
accepted: 26 04 2023
medline: 31 7 2023
pubmed: 10 5 2023
entrez: 10 5 2023
Statut: epublish

Résumé

Diet and decreased gut microbiome diversity has been associated with acute pancreatitis (AP) risk. However, differences in dietary intake, gut microbiome, and their impact on microbial end metabolites have not been studied in AP. We aimed to determine differences in (i) dietary intake (ii) gut microbiome diversity and sulfidogenic bacterial abundance, and (iii) serum short-chain fatty acid (SCFA) and hydrogen sulfide (H 2 S) concentrations in AP and control subjects. This case-control study recruited 54 AP and 46 control subjects during hospitalization. Clinical and diet data and stool and blood samples were collected. 16S rDNA sequencing was used to determine gut microbiome alpha diversity and composition. Serum SCFA and H 2 S levels were measured. Machine learning (ML) model was used to identify microbial targets associated with AP. AP patients had a decreased intake of vitamin D 3 , whole grains, fish, and beneficial eicosapentaenoic, docosapentaenoic, and docosahexaenoic acids. AP patients also had lower gut microbiome diversity ( P = 0.021) and a higher abundance of sulfidogenic bacteria including Veillonella sp. and Haemophilus sp., which were associated with AP risk. Serum acetate and H 2 S concentrations were significantly higher in the AP group ( P < 0.001 and P = 0.043, respectively). ML model had 96% predictive ability to distinguish AP patients from controls. AP patients have decreased beneficial nutrient intake and gut microbiome diversity. An increased abundance of H 2 S-producing genera in the AP and SCFA-producing genera in the control group and predictive ability of ML model to distinguish AP patients indicates that diet, gut microbiota, and their end metabolites play a key role in AP.

Identifiants

pubmed: 37162146
doi: 10.14309/ctg.0000000000000597
pii: 01720094-990000000-00156
pmc: PMC10371326
doi:

Substances chimiques

Fatty Acids, Volatile 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

e00597

Subventions

Organisme : BLRD VA
ID : I01 BX003382
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK104927
Pays : United States
Organisme : NCATS NIH HHS
ID : KL2 TR002002
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK127378
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK020595
Pays : United States

Informations de copyright

Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The American College of Gastroenterology.

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Auteurs

Cemal Yazici (C)

Division of Gastroenterology and Hepatology, Department of Medicine, University of Illinois Chicago, Chicago, Illinois, USA.

Sarang Thaker (S)

Division of Gastroenterology and Hepatology, Department of Medicine, Northwestern University, Chicago, Illinois, USA.

Karla K Castellanos (KK)

Division of Gastroenterology and Hepatology, Department of Medicine, University of Illinois Chicago, Chicago, Illinois, USA.

Haya Al Rashdan (H)

Division of Gastroenterology and Hepatology, Department of Medicine, University of Illinois Chicago, Chicago, Illinois, USA.

Yongchao Huang (Y)

Department of Biomedical Engineering, University of Illinois Chicago, Chicago, Illinois, USA.

Paya Sarraf (P)

Department of Medicine, University of Illinois Chicago, Chicago, Illinois, USA.

Brian Boulay (B)

Division of Gastroenterology and Hepatology, Department of Medicine, University of Illinois Chicago, Chicago, Illinois, USA.

Paul Grippo (P)

Division of Gastroenterology and Hepatology, Department of Medicine, University of Illinois Chicago, Chicago, Illinois, USA.

H Rex Gaskins (HR)

Department of Animal Sciences, Cancer Center at Illinois, University of Illinois Urbana-Champaign, Urbana-Champaign, Illinois, USA.

Kirstie K Danielson (KK)

Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Illinois Chicago, Chicago, Illinois, USA.

Georgios I Papachristou (GI)

Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, The Ohio State University, Columbus, Ohio, USA.

Lisa Tussing-Humphreys (L)

Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, Illinois, USA.

Yang Dai (Y)

Department of Biomedical Engineering, University of Illinois Chicago, Chicago, Illinois, USA.

Ece R Mutlu (ER)

Division of Gastroenterology and Hepatology, Department of Medicine, University of Illinois Chicago, Chicago, Illinois, USA.

Brian T Layden (BT)

Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Illinois Chicago, Chicago, Illinois, USA.
Jesse Brown VA Medical Center, Chicago, Illinois, USA.

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