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Marcotte, Bruno

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Université Laval. Institut sur la nutrition et les aliments fonctionnels



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  • PublicationRestreint
    Fish nutrients decrease expression levels of tumor necrosis factor-α in cultured human macrophages
    (American Physiological Society, 2010-02-01) Marcotte, Bruno; Marette, André; Rudkowska, Iwona; Pilon, Geneviève; Lavigne, Charles
    Numerous studies have demonstrated the beneficial effects of fish consumption on inflammatory markers. Until now, these beneficial effects of fish consumption have been mostly linked to the omega-3 fatty acids (FA). The objective of the present study was to examine, in vitro, whether expression levels of genes involved in the inflammatory response differ in human macrophages incubated with casein hydrolysates (CH) or fish protein hydrolysates (FPH) in the presence or absence of omega-3 FA compared with omega-3 FA alone. Peripheral blood monocytes differentiated into macrophages from 10 men were incubated in the presence of omega-3 FA (10 μM eicosapentaenoic acid and 5 μM docosahexaenoic acid) or CH or FPH (10, 100, 1,000 μg) with or without omega-3 FA for 48 h. Results demonstrate that expression levels of tumor necrosis factorα (TNFα) had a tendency to be lower after the addition of FPH alone or CH with omega-3 FA compared with omega-3 FA treatment. Furthermore, the combination of FPH and omega-3 FA synergistically decreased expression levels of TNFα compared to treatment with omega-3 FA or FPH alone. No difference on gene expression levels of interleukin-6 was observed between treatments. In conclusion, these preliminary results suggest that the anti-inflammatory effects of fish consumption can be explained by a synergistic effect of the omega-3 FA with the protein components of fish on TNFα expression and therefore contribute to the beneficial effects of fish consumption. Hence, follow-up studies should be performed to confirm the effects of a diet rich in FPH and omega-3 FA on serum proinflammatory cytokine concentrations. it is well described in the literature that atherosclerosis as well as insulin resistance and type 2 diabetes can be caused by chronic inflammation (18, 41). An increased level of proinflammatory cytokines may result from a variety of influences including damage to the arterial wall, accumulation of visceral body fat, macrophage infiltration in adipose tissue, and specific dietary factors. Fish consumption has demonstrated anti-inflammatory effects that are thought to be mainly due to omega-3 fatty acid (FA) content. Numerous studies with eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) supplementation reported decreased ex vivo peripheral blood mononuclear cell (PBMC) production of tumor necrosis factor-α (TNF-α) by 26% to 74%, interleukin (IL)-6 by 19% to 84%, and IL-1β by 15% to 85% in healthy individuals, yet others demonstrated that omega-3 FA did not reduce proinflammatory cytokine release (46). The large interstudy variability in response to omega-3 FA treatment is possibly due to the dose of omega-3 FA, the study duration, and/or the genetic variation of the population. Furthermore, anti-inflammatory actions of omega-3 FA have been demonstrated in cancer (8), inflammatory bowel disease (5), and other chronic diseases (46). Even if the effects of omega-3 FA on inflammation markers are inconsistent in healthy individuals, the beneficial effects of omega-3 FA for subjects with inflammatory disorders are promising. Furthermore, the literature also suggests that the favorable effects of the consumption of fish on cardiovascular risk factors may arise from its unique amino acid composition. Studies have found effects of fish proteins on blood pressure, lipoprotein profile, triglyceride (TG) levels, and insulin resistance (1, 2, 10–14, 23, 24, 27, 31, 32, 49). In addition, a human study demonstrated that cod protein consumption reduced by 24% plasma C-reactive protein (CRP) levels (40) that may be associated with improved insulin sensitivity (39) in insulin-resistant men and women. Furthermore, the synergistic effects of omega-3 FA and fish protein have been studied previously in clinical trials with fatty fish consumption. First, a study demonstrated that the regular consumption of sea bass lowered plasma TG levels and decreased inflammation markers including plasma CRP by 22.5%, IL-6 by 42.2%, and IL-8 by 25.6% in dyslipidemic subjects (47). Second, a herring-rich diet tended to lower CRP and to increase plasma high-density lipoprotein cholesterol (HDL-C) levels in overweight men (33). Despite the CRP lowering, the same study did not find any changes in vivo in oxidation or serum antioxidant status (34). Third, a recent study demonstrated that the intake of fatty fish or lean fish did not alter the expression of inflammatory genes of patients with coronary heart disease (22). However, the authors suggested that the lack of change in gene expression might be due to the ability to incorporate the omega-3 FA, the length of the study, the high variation in expression response, the use of concurrent medication, and the need for higher doses of omega-3 FA (22). Therefore, the effect of individual or synergistic effects of fish nutrients on anti-inflammatory markers is not yet clear. The anti-inflammatory effects of omega-3 FA appear to be exerted at the level of gene expression; however, the impact of fish proteins on altering proinflammatory gene expression levels is unknown. Since macrophages are the primary inflammatory cells, we hypothesize that monocyte-derived macrophages exhibit differences in expression of key genes involved in inflammation when incubated with fish protein hydrolysates (FPH), omega-3 FA, or a combination of both.
  • PublicationAccès libre
    Feeding diversified protein sources exacerbates hepatic insulin resistance via increased gut microbial branched-chain fatty acids and mTORC1 signaling in obese mice
    (Nature Publishing Group, 2021-06-07) Marcotte, Bruno; Houde, Vanessa; Daniel, Noémie; Marette, André; Tremblay, Angelo; Varin, Thibaut; Vors, Cécile; Choi, Béatrice; Ouellette, Adia; Ilkayeva, Olga; Feutry, Perrine; Ståhlman, Marcus; St-Pierre, Philippe; Bäckhed, Fredrik; Phillip J. White
    Animal models of human diseases are classically fed purified diets that contain casein as the unique protein source. We show that provision of a mixed protein source mirroring that found in the western diet exacerbates diet-induced obesity and insulin resistance by potentiating hepatic mTORC1/S6K1 signaling as compared to casein alone. These effects involve alterations in gut microbiota as shown by fecal microbiota transplantation studies. The detrimental impact of the mixed protein source is also linked with early changes in microbial production of branched-chain fatty acids (BCFA) and elevated plasma and hepatic acylcarnitines, indicative of aberrant mitochondrial fatty acid oxidation. We further show that the BCFA, isobutyric and isovaleric acid, increase glucose production and activate mTORC1/ S6K1 in hepatocytes. Our findings demonstrate that alteration of dietary protein source exerts a rapid and robust impact on gut microbiota and BCFA with significant consequences for the development of obesity and insulin resistance.