Effect of different sources of saturated and polyunsaturated fatty acids on postprandial inflammation: A double-blind randomized crossover trial

Artikel i vetenskaplig tidskrift, 2026

Background and aims Acute postprandial inflammation is a transient response to food intake and may, if repeatedly exaggerated, contribute to chronic low-grade inflammation associated with cardiometabolic disease. A high-fat meal can trigger an acute inflammatory response in the postprandial state, but the role of dietary fat composition remains unclear. The primary aim of the study was to evaluate the effect of different sources of saturated fatty acids (SFA) and Polyunsaturated fatty acids (PUFA) on the postprandial inflammatory response, and the secondary aim was to identify markers of postprandial inflammation.
Methods In a double-blind, randomized 4-way crossover trial, 18 healthy adults consumed isocaloric test meals (706 kcal) with 40 g of fat from either butter, coconut oil, flaxseed oil, or corn oil. Postprandial blood samples were collected up to 6 h. Inflammatory proteins were measured using proximity extension assay while glycoprotein acetyls (GlycA) and triacylglycerol (TG) were measured by NMR spectroscopy. Postprandial changes were analyzed with linear mixed models; markers affected by time (p < 0.05) were further studied for time × fat source interactions.
Results Twenty-one (23 %) of 93 proteins changed postprandially, across all meal challenges combined (p < 0.05 for time), including GlycA, IL-6, IL-17C, CXCL10, FGF19, and MMP1, indicating a broad but heterogeneous inflammatory response. Significant time × fat source interactions were found for GlycA (p < 0.001) and IL-17C (p = 0.022). GlycA rose more after PUFA-rich meals (corn, flaxseed) than SFA-rich meals (butter, coconut), while IL-17C was higher after flaxseed oil. Additional pairwise differences were observed but were inconsistent across markers and fat sources. There were no differences in plasma TG concentration between fat sources.
Conclusions While several markers of inflammation were altered after the high-fat meal, no consistent directional pattern was observed that would favor a specific fat source. PUFA-rich meals elicited slightly stronger inflammatory responses than SFA-rich meals, but overall, fat source had a modest influence. Further research is needed to clarify the clinical relevance and potential implications of the findings.
Clinical trial registry The study was registered at Clinicaltrials.gov (NCT05674708).