Krista A. Power

University of Ottawa

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Jennifer M. Monk

University of Guelph

Lindsay E. Robinson

University of Guelph

Lilian U. Thompson

University of Toronto

Dion Lepp

Agriculture and Agri-Food Canada

Wenqing Wu

Shanghai Zhangjiang Laboratory

Danyelle M. Liddle

University of Guelph

Amber L. Hutchinson

University of Guelph

Daniela Gräf

Max Rubner Institut

Rong Tsao

Agriculture and Agri-Food Canada

David W.L.

University of Guelph

Cooperative Institutions

University of Guelph

University of Toronto

University of Ottawa

Agriculture and Agri-Food Canada

Universidade Estadual Paulista (Unesp)

Hospital for Sick Children

Royal Marsden NHS Foundation Trust

University College London

Karolinska Institutet

Royal Marsden Hospital

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Lignan-rich sesame seed negates the tumor-inhibitory effect of tamoxifen but maintains bone health in a postmenopausal athymic mouse model with estrogen-responsive breast tumors

Menopause The Journal of The North American Menopause Society (2007)

Sandra M. Sacco Jianmin Chen Krista A. Power Wendy E. Ward Lilian U. Thompson

In Brief Objective: Flaxseed, the richest source of mammalian lignan precursors, enhances the tumor growth-inhibitory effect of tamoxifen while exerting no adverse effects on other estrogen-responsive tissues such as bone. Ingestion of sesame seed produces mammalian lignans comparable with flaxseed, but its anticancer potential is unknown. This study determined the interactive effects of sesame seed and tamoxifen on established MCF-7 tumor growth and bone health in ovariectomized athymic mice simulating a postmenopausal condition. Design: Mice with established MCF-7 tumors were treated for 8 weeks with (1) basal diet (negative control), (2) 10% sesame seed, (3) basal diet + tamoxifen implant, (4) 10% sesame seed + tamoxifen implant, or (5) basal diet + estrogen implant (positive control). Weekly palpable tumor size, final tumor weight, cell proliferation, and apoptosis were measured. Bone mineral content, bone mineral density, and biomechanical strength testing were performed on the femur and lumbar vertebrae. Results: Sesame seed induced regression of established tumor size similar to the negative control but tended to negate the tumor-inhibitory effect of tamoxifen, in part by reducing apoptosis. Sesame seed combined with tamoxifen induced higher bone mineral content, bone mineral density, and biomechanical strength in the femur and lumbar vertebrae than either treatment alone. A significant positive relationship was found between final tumor weight and bone strength parameters. Conclusions: Sesame seed is not protective and negatively interferes with tamoxifen in inducing regression of established MCF-7 tumor size but beneficially interacts with tamoxifen on bone in ovariectomized athymic mice. Lignan-rich flaxseed protects against breast cancer and enhances the tumor-inhibitory effect of the breast cancer drug tamoxifen while exerting no adverse effects on estrogen-sensitive tissues such as the bone. This study showed for the first time that lignan-rich sesame seed is not protective and negatively interferes with tamoxifen in ovariectomized athymic mice with established MCF-7 tumors, but enhances the protective effect of tamoxifen on bone health.

10.1097/gme.0b013e3180479901

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Ground flaxseed reverses protection of a reduced-fat diet against Citrobacter rodentium-induced colitis

AJP Gastrointestinal and Liver Physiology (2018)

Pekka Määttänen Eberhard Lurz Steven R. Botts Richard Wu Celine Yeung

Flaxseed is high in ω-3 polyunsaturated fatty acids, fiber, and lignans known to lower cholesterol levels. However, its use for prevention or treatment of inflammatory bowel diseases has yielded mixed results, perhaps related to dietary interactions. In this study, we evaluated the impact of ground flaxseed supplementation on the severity of Citrobacter rodentium-induced colitis in the setting of either a high-fat (HF, ~36%kcal) or reduced-fat (RF, ~12%kcal) diet. After weaning, C57BL/6 mice ( n = 8-15/treatment) were fed ground flaxseed (7 g/100 g diet) with either HF (HF Flx) or RF (RF Flx) diets for 4 wk before infection with C. rodentium or sham gavage. Weight changes, mucosal inflammation, pathogen burden, gut microbiota composition, tissue polyunsaturated fatty acids, and cecal short-chain fatty acids were compared over a 14-day infection period. The RF diet protected against C. rodentium-induced colitis, whereas the RF Flx diet increased pathogen burden, exacerbated gut inflammation, and promoted gut dysbiosis. When compared with the RF diet, both HF and HF Flx diets resulted in more severe pathology in response to C. rodentium infection. Our findings demonstrate that although an RF diet protected against C. rodentium-induced colitis and associated gut dysbiosis in mice, beneficial effects were diminished with ground flaxseed supplementation. NEW & NOTEWORTHY Our results demonstrate a strong protective effect of a reduced-fat diet against intestinal inflammation, dysbiosis, and pathogen burden during Citrobacter rodentium-induced colitis. However, ground flaxseed supplementation in the setting of a reduced-fat diet exacerbated colitis despite higher levels of intestinal n-3 polyunsaturated fatty acids and cecal short-chain fatty acids.

Citrobacter rodentium

Dysbiosis

10.1152/ajpgi.00101.2018

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Lentil-supplemented diets prime the colonic microenvironment to attenuate DSS-induced colitis severity in C57Bl/6 mice

Daniela Gräf Jennifer M. Monk Wenqing Wu L. McGillis Lindsay Robinson

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Dietary sources of lignans and isoflavones modulate responses to estradiol in estrogen reporter mice

Molecular Nutrition & Food Research (2009)

Pauliina Damdimopoulou Krista A. Power Teija T. Hurmerinta Tarja Nurmi Paul T. van der Saag

Dietary phytoestrogens, such as the lignan metabolite enterolactone (ENL) and the isoflavone genistein (GEN), are suggested to modulate the risk of estrogen-dependent disease (e.g., breast cancer) through regulation of estrogen signaling. However, the effects of complex food items containing lignans or isoflavones on estrogen receptor (ER) transactivation have not been assessed so far. In this study, the modulation of ER-mediated signaling by dietary sources of lignans (cereals and flaxseed) and isoflavones (soy) was studied in vivo. Adult ovariectomized 3 x ERE-luciferase (luc) reporter mice received isocaloric diets supplemented with flaxseed, rye, wheat, or soy for 40 h or two weeks, and an additional group of mice was challenged with 17beta-estradiol (E(2)) following the two-week dietary intervention. In non-E(2)-treated mice, soy diet induced luc expression in liver, mammary gland, and pituitary gland while the other diets had no effects. Interestingly, all diets modulated the E(2)-induced luc expression. In particular rye diet efficiently reduced E(2)-induced luc expression as well as uterine growth, the hallmark of estrogen action in vivo. It is concluded that dietary sources of lignans and isoflavones can modulate estrogen signaling in vivo. The results suggest intriguing possibilities for the modulation of the risk of estrogen-dependent diseases by dietary means.

Enterolactone

Biochanin A

10.1002/mnfr.200800487

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Fish Oil-Derived Long-Chain n-3 Polyunsaturated Fatty Acids Reduce Expression of M1-Associated Macrophage Markers in an ex vivo Adipose Tissue Culture Model, in Part through Adiponectin

Frontiers in Nutrition (2015)

Anna A. De Boer Jennifer M. Monk Danyelle M. Liddle Krista A. Power David W.L.

Adipose tissue (AT) macrophages (ATM) play a key role in obesity-associated pathologies, and their phenotype can be influenced by the local tissue microenvironment. Interestingly, long-chain n-3 polyunsaturated fatty acids (LC n-3 PUFA) and the LC n-3 PUFA-upregulated adipokine, adiponectin (Ad), may mitigate excessive ATM inflammatory M1-polarization responses. However, to what extent LC n-3 PUFA and Ad work in concert to affect macrophage phenotype has not been examined. Thus, we used an established ex vivo AT organ culture model using visceral AT from mice fed a control (CON; 10% w/w safflower oil) n-6 PUFA-rich diet or an isocaloric fish oil (FO; 3% w/w menhaden oil + 7% w/w safflower oil)-derived LC n-3 PUFA-rich diet to generate AT conditioned media (ACM). We then evaluated if CON or FO ACM affected macrophage polarization markers in a model designed to mimic acute [18 h ACM plus lipopolysaccharide (LPS) for the last 6 h] or chronic (macrophages treated with LPS-challenged CON or FO ACM for 24 h) inflammation ± Ad-neutralizing antibody and the LPS-neutralizing agent, polymyxin B. In the acute inflammation model, macrophages treated with FO ACM had decreased lipid uptake and mRNA expression of M1 markers (Nos2, Nfκb, Il6, Il18, Ccl2, and Ccl5) compared with CON ACM (p ≤ 0.05); however, these effects were largely attenuated when Ad was neutralized (p > 0.05). Furthermore, in the chronic inflammation model, macrophages treated with FO ACM had decreased mRNA expression of M1 markers (Nos2, Tnfα, Ccl2, and Il1β) and IL-6 and CCL2 secretion (p ≤ 0.05); however, some of these effects were lost when Ad was neutralized, and were further exacerbated when both Ad and LPS were neutralized. Taken together, this work shows that LC n-3 PUFA and Ad work in concert to suppress certain M1 macrophage responses. Thus, future strategies to modulate the ATM phenotype should consider the role of both LC n-3 PUFA and Ad in mitigating obese AT inflammation.

Ex vivo

10.3389/fnut.2015.00031

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Obesity Promotes Marrow-Derived Myeloid Cell Accumulation while Exercise Reduces Proliferative Signaling in Colon Cancer

Medicine & Science in Sports & Exercise (2024)

James J. Vanhie Lisa Ek Orloff ALICE TATE Cole Goode Nicolás Collao

ABSTRACT Purpose Obesity increases colon cancer risk that has been previously linked to marrow-derived myeloid cells. We previously demonstrated that exercise training (EX) prevents colon cancer initiation, potentially through reduced myelopoiesis. However, it remains unknown whether early myeloid cell accumulation and inflammation in the colon precedes carcinogenesis with high-fat diet (HFD)-induced obesity, and if EX can attenuate these effects. We hypothesized that obesity would promote colon carcinogenesis that was preceded by myeloid cell accumulation and inflammation that would be attenuated by EX. Methods C57BL/6 mice were randomized to a HFD or control (CON) diet for 8 weeks. The HFD mice switched to CON diet and all mice were given intraperitoneal injections of azoxymethane (AOM) to induce colon cancer and randomized into EX or sedentary (SED) conditions. Results HFD mice developed more aberrant crypt foci (ACF), a marker for early carcinogenesis, compared with CON ( P < 0.01), and EX developed fewer ACF compared with SED ( P < 0.0001). Marrow-derived ( P < 0.001) CD206 + macrophages were elevated in HFD compared with CON at study week 16 ( P < 0.01). Marrow-derived CD206 − macrophages ( P < 0.05) and marrow-derived ( P < 0.05) CD206 + macrophages were more abundant in HFD compared with CON at study week 42. EX did not alter colon immune cell populations. β-catenin protein was higher in HFD compared with CON at study week 42 ( P < 0.05), and STAT3 protein content was lower at study week 28 with EX compared with SED ( P < 0.05). Conclusions The results suggest that obesity promotes colon ACF formation, potentially through early inflammatory myeloid cell accumulation. Despite attenuating ACF, EX did not alter myeloid cell accumulation in the colon, suggesting that EX inhibits ACF formation through alternative mechanisms which may include reduced β-catenin and STAT3 signaling.

10.1249/mss.0000000000003572

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Genistein alone and in combination with the mammalian lignans enterolactone and enterodiol induce estrogenic effects on bone and uterus in a postmenopausal breast cancer mouse model

Bone (2006)

Krista A. Power Wendy E. Ward Jianmin Chen Niina Saarinen Lilian U. Thompson

Enterolactone

10.1016/j.bone.2005.12.015

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Dietary flaxseed intake exacerbates acute colonic mucosal injury and inflammation induced by dextran sodium sulfate

AJP Gastrointestinal and Liver Physiology (2014)

Leila Zarepoor Jenifer T. Lu Claire Zhang Wenqing Wu Dion Lepp

Flaxseed (FS), a dietary oilseed, contains a variety of anti-inflammatory bioactives, including fermentable fiber, phenolic compounds (lignans), and the n-3 polyunsaturated fatty acid (PUFA) α-linolenic acid. The objective of this study was to determine the effects of FS and its n-3 PUFA-rich kernel or lignan- and soluble fiber-rich hull on colitis severity in a mouse model of acute colonic inflammation. C57BL/6 male mice were fed a basal diet (negative control) or a basal diet supplemented with 10% FS, 6% kernel, or 4% hull for 3 wk prior to and during colitis induction via 5 days of 2% (wt/vol) dextran sodium sulfate (DSS) in their drinking water (n = 12/group). An increase in anti-inflammatory metabolites (hepatic n-3 PUFAs, serum mammalian lignans, and cecal short-chain fatty acids) was associated with consumption of all FS-based diets, but not with anti-inflammatory effects in DSS-exposed mice. Dietary FS exacerbated DSS-induced acute colitis, as indicated by a heightened disease activity index and an increase in colonic injury and inflammatory biomarkers [histological damage, apoptosis, myeloperoxidase, inflammatory cytokines (IL-6 and IL-1β), and NF-κB signaling-related genes (Nfkb1, Ccl5, Bcl2a1a, Egfr, Relb, Birc3, and Atf1)]. Additionally, the adverse effect of the FS diet was extended systemically, as serum cytokines (IL-6, IFNγ, and IL-1β) and hepatic cholesterol levels were increased. The adverse effects of FS were not associated with alterations in fecal microbial load or systemic bacterial translocation (endotoxemia). Collectively, this study demonstrates that although consumption of a 10% FS diet enhanced the levels of n-3 PUFAs, short-chain polyunsaturated fatty acids, and lignans in mice, it exacerbated DSS-induced colonic injury and inflammation.

Basal (medicine)

10.1152/ajpgi.00253.2013

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Cooked Red Lentils Dose-Dependently Modulate the Colonic Microenvironment in Healthy C57Bl/6 Male Mice

Nutrients (2019)

Daniela Gräf Jennifer M. Monk Dion Lepp Wenqing Wu L. McGillis

Dietary pulses, including lentils, are protein-rich plant foods that are enriched in intestinal health-promoting bioactives, such as non-digestible carbohydrates and phenolic compounds. The aim of this study was to investigate the effect of diets supplemented with cooked red lentils on the colonic microenvironment (microbiota composition and activity and epithelial barrier integrity and function). C57Bl/6 male mice were fed one of five diets: a control basal diet (BD), a BD-supplemented diet with 5, 10 or 20% cooked red lentils (by weight), or a BD-supplemented diet with 0.7% pectin (equivalent soluble fiber level as found in the 20% lentil diet). Red lentil supplementation resulted in increased: (1) fecal microbiota α-diversity; (2) abundance of short-chain fatty acid (SCFA)-producing bacteria (e.g., Prevotella, Roseburia and Dorea spp.); (3) concentrations of fecal SCFAs; (4) mRNA expression of SCFA receptors (G-protein-coupled receptors (GPR 41 and 43) and tight/adherens junction proteins (Zona Occulden-1 (ZO-1), Claudin-2, E-cadherin). Overall, 20% lentil had the greatest impact on colon health outcomes, which were in part explained by a change in the soluble and insoluble fiber profile of the diet. These results support recent public health recommendations to increase consumption of plant-based protein foods for improved health, in particular intestinal health.

Roseburia

Red meat

Adherens junction

Prevotella

10.3390/nu11081853

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Assessing the Effects of Acute and Chronic Whole Apple Consumption on Biomarkers of Inflammation in Overweight and Obese Adults (P21-011-19)

Current Developments in Nutrition (2019)

Danyelle M. Liddle Xinjie Lin Liam Cox Emily Ward Krista A. Power

Systemic low-grade inflammation mechanistically links obesity to impairments in the metabolic processes central to the development of type 2 diabetes and cardiovascular disease. This phenomenon is promoted by digestion of a high-fat meal, whereas whole foods with proposed anti-inflammatory actions, such as apples, may be beneficial. Thus, the current studies aimed to assess the effects of acute and chronic consumption of whole apples on biomarkers of inflammation in overweight and obese adults. Overweight or obese adults in otherwise good health were recruited. With n = 26 (17 female/9 male; mean age 45.5 ± 3.1 y; mean BMI 34.1 ± 0.2 kg/m2), a randomized, crossover trial was conducted to assess the effects of acute (one time) consumption of 3 whole Gala apples (∼200 g) on the 6 h postprandial inflammatory response (e.g., plasma gut-derived lipopolysaccharide (LPS), cytokines) to an oral fat tolerance test (1 g fat/kg body weight). Fasting and 4 h postprandial peripheral blood mononuclear cells (PBMCs) were also isolated from whole blood and stimulated with 10 ng/mL LPS for 24 h to measure secreted cytokines. With n = 46 (32 female/14 male; mean age, 46.2 ± 2.2 y; mean BMI 33.5 ± 0.8 kg/m2), a parallel-arm, randomized, controlled trial was conducted to assess the effects of chronic (6 week) consumption of 3 whole Gala apples per day (∼200 g) on fasting inflammatory markers. Acute apple consumption decreased 4 h postprandial unstimulated (IL-1β, granulocyte-macrophage colony-stimulating factor (GM-CSF), macrophage inflammatory protein (MIP)-1β, TNF-α) and LPS-stimulated (IL-6, TNF-α) PBMC-secreted inflammatory cytokines (P < 0.05, n = 18). Similarly, chronic apple consumption decreased fasting unstimulated (IL-6) and LPS-stimulated (IL-6, INF-γ, TNF-α) PBMC-secreted inflammatory cytokines (P < 0.05; n = 16–18/group), as well as plasma IL-6 (P < 0.05, n = 22/group). Both acute and chronic whole apple consumption may be an effective dietary strategy to mitigate the obesity-associated inflammation that precedes and exacerbates metabolic disease risk. Ontario Ministry of Agriculture, Food & Rural Affairs; Ontario Apple Growers.

Crossover study

10.1093/cdn/nzz041.p21-011-19

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Citations (1)