Center for Botanical Lipids and Inflammatory Disease Prevention

Pumpkin Center, NC, United States

Center for Botanical Lipids and Inflammatory Disease Prevention

Pumpkin Center, NC, United States
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Sergeant S.,Center for Botanical Lipids and Inflammatory Disease Prevention | Hugenschmidt C.E.,Center for Diabetes Research | Rudock M.E.,Center for Human Genomics | Ivester P.,Center for Botanical Lipids and Inflammatory Disease Prevention | And 6 more authors.
British Journal of Nutrition | Year: 2012

Over the past 50 years, increases in dietary n-6 PUFA, such as linoleic acid, have been hypothesised to cause or exacerbate chronic inflammatory diseases. The present study examines an individual's innate capacity to synthesise n-6 long-chain PUFA (LC-PUFA) with respect to the fatty acid desaturase (FADS) locus in Americans of African and European descent with diabetes or the metabolic syndrome. Compared with European Americans (EAm), African Americans (AfAm) exhibited markedly higher serum levels of arachidonic acid (AA) (EAm 79 (sd 21), AfAm 98 (sd 19) % of total fatty acids; P < 229 × 10 - 9) and the AA:n-6-precursor fatty acid ratio, which estimates FADS1 activity (EAm 54 (sd 22), AfAm 69 (sd 22); P = 144 × 10 - 5). In all, seven SNP mapping to the FADS locus revealed strong association with AA, EPA and dihomo-γ-linolenic acid (DGLA) in the EAm. Importantly, EAm homozygous for the minor allele (T) had significantly lower AA levels (TT 63 (sd 10); GG 85 (sd 21); P = 30 × 10 - 5) and AA:DGLA ratios (TT 34 (sd 08), GG 65 (sd 23); P = 22 × 10 - 7) but higher DGLA levels (TT 19 (sd 04), GG 14 (sd 04); P = 33 × 10 - 7) compared with those homozygous for the major allele (GG). Allele frequency patterns suggest that the GG genotype at rs174537 (associated with higher circulating levels of AA) is much higher in AfAm (081) compared with EAm (046). Similarly, marked differences in rs174537 genotypic frequencies were observed in HapMap populations. These data suggest that there are probably important differences in the capacity of different populations to synthesise LC-PUFA. These differences may provide a genetic mechanism contributing to health disparities between populations of African and European descent. © The Authors 2011.

Lee T.C.,Medical Center Blvd | Lee T.C.,Center for Botanical Lipids and Inflammatory Disease Prevention | Ivester P.,Medical Center Blvd | Ivester P.,Center for Botanical Lipids and Inflammatory Disease Prevention | And 8 more authors.
Lipids in Health and Disease | Year: 2014

Background: Ingestion 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. Methods: Fifty-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. Results: Compliance 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. Conclusion: Short-term dietary supplementation with BO and FO improved biomarkers associated with T2D/metabolic syndrome. © 2014 Lee et al.; licensee BioMed Central.

Sergeant S.,Center for Botanical Lipids and Inflammatory Disease Prevention | Sergeant S.,Medical Center Blvd | Ruczinski I.,Johns Hopkins University | Ivester P.,Center for Botanical Lipids and Inflammatory Disease Prevention | And 8 more authors.
British Journal of Nutrition | Year: 2016

Numerous studies have examined relationships between disease biomarkers (such as blood lipids) and levels of circulating or cellular fatty acids. In such association studies, fatty acids have typically been expressed as the percentage of a particular fatty acid relative to the total fatty acids in a sample. Using two human cohorts, this study examined relationships between blood lipids (TAG, and LDL, HDL or total cholesterol) and circulating fatty acids expressed either as a percentage of total or as concentration in serum. The direction of the correlation between stearic acid, linoleic acid, dihomo-γ-linolenic acid, arachidonic acid and DHA and circulating TAG reversed when fatty acids were expressed as concentrations v. a percentage of total. Similar reversals were observed for these fatty acids when examining their associations with the ratio of total cholesterol:HDL-cholesterol. This reversal pattern was replicated in serum samples from both human cohorts. The correlations between blood lipids and fatty acids expressed as a percentage of total could be mathematically modelled from the concentration data. These data reveal that the different methods of expressing fatty acids lead to dissimilar correlations between blood lipids and certain fatty acids. This study raises important questions about how such reversals in association patterns impact the interpretation of numerous association studies evaluating fatty acids and their relationships with disease biomarkers or risk. © The Authors 2015 This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence (, which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited..

Arm J.P.,Brigham and Women's Hospital | Arm J.P.,Harvard University | Arm J.P.,Novartis | Boyce J.A.,Brigham and Women's Hospital | And 17 more authors.
Lipids in Health and Disease | Year: 2013

Background: Dietary supplementation with botanical oils that contain n-6 and n-3 eighteen carbon chain (18C)-PUFA such as γ linolenic acid (GLA, 18:3n-6), stearidonic acid (SDA, 18:4n-3) and α linolenic acid (ALA, 18:3n-3) have been shown to impact PUFA metabolism, alter inflammatory processes including arachidonic acid (AA) metabolism and improve inflammatory disorders. Methods. The diet of mild asthmatics patients was supplemented for three weeks with varying doses of two botanical seed oils (borage oil [Borago officinalis, BO] and echium seed oil [Echium plantagineum; EO]) that contain SDA, ALA and GLA. A three week wash out period followed. The impact of these dietary manipulations was evaluated for several biochemical endpoints, including in vivo PUFA metabolism and ex vivo leukotriene generation from stimulated leukocytes. Results: Supplementation with several EO/BO combinations increased circulating 20-22 carbon (20-22C) PUFAs, including eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and dihommo-gammalinolenic acid (DGLA), which have been shown to inhibit AA metabolism and inflammation without impacting circulating AA levels. BO/EO combinations also inhibited ex vivo leukotriene generation with some combinations attenuating cysteinyl leukotriene generation in stimulated basophils by >50% and in stimulated neutrophils by >35%. Conclusions: This study shows that dietary supplementation with BO/EO alters 20-22C PUFA levels and attenuates leukotriene production in a manner consistent with a reduction in inflammation. © 2013 Arm et al.; licensee BioMed Central Ltd.

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