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Interorgan cross talk between fatty acid metabolism, tissue inflammation, and FADS2 genotype in humans with obesity
Author(s) -
Vaittinen Maija,
Männistö Ville,
Käkelä Pirjo,
Ågren Jyrki,
Tiainen Mika,
Schwab Ursula,
Pihlajamäki Jussi
Publication year - 2017
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.21753
Subject(s) - fads2 , inflammation , polyunsaturated fatty acid , adipose tissue , medicine , fatty acid metabolism , endocrinology , eicosapentaenoic acid , genotype , obesity , fatty acid , metabolism , biology , biochemistry , docosahexaenoic acid , gene
Objective Fatty acid (FA) composition affects obesity‐associated low‐grade inflammation. It has been shown that the fatty acid desaturase ( FADS ) 2 gene polymorphism associates with FA metabolism and adipose tissue (AT) inflammation. This study aimed to investigate the relationship between FA metabolism and inflammation in different tissues and the possible interorgan cross talk. Methods Cross‐sectional baseline data from 155 individuals with obesity (both male and female) participating in the Roux‐en‐Y gastric bypass operation in the ongoing Kuopio Obesity Surgery Study were used. Gas chromatograph for FA composition, liver histology, and targeted RNA expression for gene expression profile were performed. Results It was demonstrated that the saturated fatty acid (SFA) proportion in AT correlated positively with inflammation in subcutaneous AT (SAT) and visceral AT (VAT) but not in the liver, while the monounsaturated fatty acid (MUFA) proportion in SAT and VAT correlated negatively with AT inflammation. Notably, there was a positive correlation between AT n‐6 polyunsaturated fatty acids (PUFAs), but not AT SFAs or MUFAs, and liver inflammation. This correlation was modified by the FADS2 genotype. Conclusions The AT FA profile relates with AT inflammation. Additionally, there seems to be a complex interaction, partly regulated by the FADS2 genotype, regulating the interaction between FAs in AT and liver inflammation.