Zgadzam się
Nasza strona zapisuje niewielkie pliki tekstowe, nazywane ciasteczkami (ang. cookies) na Twoim urządzeniu w celu lepszego dostosowania treści oraz dla celów statystycznych. Możesz wyłączyć możliwość ich zapisu, zmieniając ustawienia Twojej przeglądarki. Korzystanie z naszej strony bez zmiany ustawień oznacza zgodę na przechowywanie cookies w Twoim urządzeniu.
DOAJ (Directory of Open Access Journals); • Google Scholar;; • Dimensions; • Chemical Abstracts Service (CAS) • SAO/NASA Astrophysics Data System (ADS); PubMed Central (PMC);
Efekt badań statutowych
NIE
Finansowanie:
This work was supported by the Medical University of Lublin DS. number 675 and the Department of Biological Sciences, University of Limerick. The research used an HPLC-qTOF system purchased as part of the project: “Research Centre for Environmentally Friendly and Energy-Saving Materials and Technologies (CeBMaT)” under the Smart Growth Operational Programme 2014–2020, co-financed by the European Regional Development Fund, contract no. POIR.04.02.0000-D009/20.
Inflammatory bowel diseases (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), are characterized by chronic intestinal inflammation and significant clinical variability. Growing evidence suggests that disruptions in systemic lipid metabolism play a role in IBD pathophysiology; however, detailed analysis of circulating fatty acids and arachidonic acid–derived lipid mediators in UC and CD remains limited. Therefore, in this cross-sectional observational study, we measured plasma fatty acids and arachidonic acid–derived oxylipins in patients with UC, patients with CD, and healthy controls. The study analysed 46 patients with UC and 16 with CD, for a total of 62 patients with IBD (UC + CD). These patients were compared to 40 healthy controls. Plasma fatty acids and arachidonic acid–derived oxylipins were measured using targeted high-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (HPLC–QTOF–MS). Associations with disease phenotype, sex, disease activity, and pharmacological treatment were analyzed. Both UC and CD showed a global reduction in circulating medium- and long-chain fatty acids compared to controls. Plasma arachidonic acid levels were significantly lower in both diseases, with a more notable reduction in CD. UC was characterized by a selective loss of arachidonic acid epoxide metabolites, while CD exhibited increased levels of alternative arachidonic acid–derived metabolites, with some sex-specific differences. Most lipid changes were not significantly associated with traditional inflammatory markers or disease activity. In exploratory subgroup comparisons, some CD patients receiving biological therapy or corticosteroids exhibited selected fatty acid levels closer to those observed in healthy controls. IBD is linked to disease-specific disruptions in systemic fatty acid profiles and arachidonic acid metabolism. Distinct patterns of lipid alterations were observed in UC and CD, highlighting lipid metabolism as an additional aspect of IBD pathophysiology. These exploratory findings may help identify candidate lipid markers for evaluation in larger, independently validated studies
