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Table 1 Krill oil (KO) supplementation increased the metabolites involved in pro-resolving pathways, particularly the biosynthesis of E-series resolvins. Fold change was calculated based on normalized peak intensities in Citrobacter rodentium induced colitis mice (CM) divided by those in healthy control mice (Down dysregulation) or those in KO divided by CM (Up dysregulation). Pathway: A: aspirin triggered resolvin E biosynthesis; B, aspirin-triggered lipoxin biosynthesis; C, lipoxin biosynthesis; and D, leukotriene biosynthesis

From: Mechanistic insights into the attenuation of intestinal inflammation and modulation of the gut microbiome by krill oil using in vitro and in vivo models

Metabolite

Pathway*

Fold change

P value

Dysregulation

m/z

RT

(5S)-HPETE

D*

0.33

0.0004

Down

381.2270

3.974

(15R)-hydroxyeicosapentaenoate

B*, C**

0.36

0.0022

Down

365.2321

4.474

(5S)-HPETE

D*

0.40

0.0024

Down

395.2428

5.266

(5Z,8Z,11Z,14Z,17Z)-icosapentaenoate

A**

0.20

0.0037

Down

347.2217

7.754

15 [epi-] lipoxin A4/B4

B*, C**

0.37

0.0031

Down

411.2375

4.481

18R-hydroxy-eicosapentaenoate

A**, C**, D*

0.34

0.0020

Down

363.2167

4.736

5S hydro(peroxy),18R-hydroxy-eicosapentaenoate

A**

0.25

0.0009

Down

349.2010

5.702

Resolvin E1

A**

0.29

0.0023

Down

409.2217

3.840

15S-hydroxypentaenoate

B**, C***

1.70

0.0406

Up

340.2020

9.158

leukotriene A4

A*, B**, C***

1.68

0.0067

Up

363.2167

5.253

Resolvin E2

A*, B**, C***

1.79

0.0315

Up

315.1957

7.663

  1. m/z mass-to-charge ratio, RT retention time in min
  2. ***p < 0.001; **p < 0.01; *p < 0.05.