BackgroundIngestion of polyunsaturated fatty acids (PUFAs) has been proposed to influence several chronic diseases including coronary heart disease (CHD) and type-2 diabetes (T2D).There is strong evidence that omega-3 (n-3) PUFAs provide protection against CHD and biomarkers of atherosclerosis. In contrast, there is more limited and inconsistent data for T2D. Few studies have examined the impact of n-3 PUFA-containing botanical oils on T2D.MethodsFifty-nine subjects with early-stageT2D or metabolic syndrome participated in an 8-week, randomized, single-blind, parallel intervention study and were provided PUFA-containing oils. Individuals received either corn oil (CO), a botanical oil (BO) combination (borage [Borago officinalis L.]/echium oil [Echium plantagineum L.]) or fish oil (FO). The BO combination was enriched in alpha-linolenic, gamma-linolenic, and stearidonic acids and the FO in eicosapentaenoic and docosahexaenoic acids. Serum fatty acids and other serum lipids(triglycerides and total, HDL and LDL cholesterol), as well as markers of inflammation (leptin, and C-reactive protein) and glucose regulation (glucose and hemoglobin A1c) were assessed from fasting participants at baseline and after the intervention.ResultsCompliance was verified by expected increases in specific PUFAs in each of the three oil arms. Participants in the CO group showed no differences in serum lipids, markers of inflammation or glucose regulation between pre- and post-treatment measures. Supplementation with BO significantly lowered total and LDL cholesterol levels and FO reduced serum triglycerides, hemoglobin A1c and increased HDL-cholesterol.ConclusionShort-term dietary supplementation with BO and FO improved biomarkers associated with T2D/metabolic syndrome.Trial registrationClinicaltrial.gov NCT01145066

Background: Genetic variants in the FADS cluster are determinants of arachidonate synthesis, but their role in eicosanoid generation remains unclear. Results: FADS SNP, rs174537 is associated with leukotriene B 4 and 5-HETE production from stimulated human blood. Conclusion: A FADS SNP affects the synthesis of 5-lipoxygenase products. Significance: FADS variation may influence inflammation via eicosanoid biosynthesis.

BACKGROUND In vitro and experimental animal studies have demonstrated that high levels of omega‐6 (n‐6) polyunsaturated fatty acids (PUFAs) and high ratios of n‐6 to omega‐3 (n‐3) PUFAs are strongly associated with the development and progression of prostate cancer (PCA). However, epidemiological studies in humans have demonstrated inconsistent findings linking dietary PUFAs and PCA risk. We hypothesize that genetic and epigenetic variations within the fatty acid desaturase ( FADS ) gene cluster produce gene–diet interactions that may explain these disparate findings. This study tested the relationship of the genotype of a single nucleotide polymorphism, rs174537, and the methylation status of a CpG site, cg27386326, with PUFA composition, and markers of PUFA biosynthesis in PCA tissue. METHODS Sixty PCA specimens from patients undergoing radical prostatectomy were genotyped, pyrosequenced and quantitated for fatty acids (FAs). RESULTS Long‐chain (LC)‐PUFAs, such as arachidonic acid (ARA), were abundant in these specimens, with ARA accounting for 15.8% of total FAs. In addition, there was a positive association of the G allele at rs174537 with concentrations of ARA and adrenic acid and ratios of products to precursors within the n‐6 PUFA pathway such that specimens from homozygous G individuals exhibited increasingly higher values as compared to specimens from heterozygous individuals and homozygous T individuals. Finally, the methylation status of cg27386326 was inversely correlated with tissue concentrations of LC‐PUFAs and markers of LC‐PUFA biosynthesis. CONCLUSIONS These data reveal that genetic and epigenetic variations within the FADS cluster are highly associated with LC‐PUFA concentrations and LC‐PUFA biosynthetic capacity in PCA tissue. They also raise the potential that gene–PUFA interactions play an important role in PCA risk and severity. Prostate 76:1182–1191, 2016 . © 2016 The Authors. The Prostate published by Wiley Periodicals, Inc.

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