Fatty Acids, IL6 and TNFα Polymorphisms: An Example of Nutrigenetics in Crohn's Disease

Guerreiro, Catarina Sousa; Ferreira, Paula; Tavares, L.; Santos, Paula Moura; Neves, M. Manuela; Brito, Miguel; Cravo, Marília

doi:10.1038/ajg.2009.313

Cited by 56 publications

(38 citation statements)

References 30 publications

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“…Later on, we also observed that a high intake of monounsaturated fat was associated with more active disease. 15 In the present study, although in univariate analysis intake of monounsaturated fat was associated with increased risk of presenting a Z-score lower than À2.0, multivariate analysis did not show that fat intake was an independent risk factor for MBD. Nonetheless, further studies are needed to clarify whether the amount and type of fat intake might influence the prevalence of MBD in patients with CD.…”

Section: Discussioncontrasting

confidence: 80%

“…In a previous study performed in this same population, we observed that a high intake of total, monounsaturated fat, as well as a higher ratio of n6/n3 polyunsaturated fatty acids, were associated with a more active disease. 15 Fat intake is now regarded as a potent immunomodulatory therapy in patients with CD [30][31][32][33][34][35] either by modulating eicosanoid synthesis, by altering cell membrane fluidity, cell signal transduction, or even gene expression. More interestingly, Gassull et al, 30 in a randomized controlled study performed in patients with active CD, examined the effects of an n-6-versus an n-9-enriched diet as compared with conventional therapy with steroids.…”

Section: Discussionmentioning

confidence: 99%

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Risk factors for metabolic bone disease in Crohnʼs disease patients

Cravo

Guerreiro

Santos

et al. 2010

Inflammatory Bowel Diseases

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Section: Discussioncontrasting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Risk factors for metabolic bone disease in Crohnʼs disease patients

Cravo

Guerreiro

Santos

et al. 2010

Inflammatory Bowel Diseases

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“…by guest, on May 10, 2018 www.jlr.org Downloaded from plain from the current dataset and are not in line with reports from other disorders that have been associated with elevated immune parameters such as depression ( 19 ) and Crohn's disease ( 48 ). Of note is that in the latter study, the elevated -6: -3 ratio was related to specifi c cytokine genotypes.…”

Section: Discussioncontrasting

confidence: 38%

Marked elevations in pro-inflammatory polyunsaturated fatty acid metabolites in females with irritable bowel syndrome

Clarke

Fitzgerald

Hennessy

et al. 2010

Journal of Lipid Research

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Irritable bowel syndrome (IBS) is a common and potentially disabling, though nonfatal, medical disorder that can affect up to 20% of the population. It is the most common functional gastrointestinal disorder referred to gastroenterologists ( 1 ). Although it has evolved over the years in terms of nomenclature ( 2, 3 ), classifi cation ( 4-6 ), and appreciation of its frequency ( 7 ), a poor understanding of disease pathophysiology has remained a constant. According to the Rome III criteria, a symptom-based classifi cation system, the disease-defi ning symptom profi le encompasses abdominal pain and an altered bowel habit, with distension, bloating, and a variety of disturbances in defecatory function being additional features ( 8 ).The disorder is increasingly viewed as a disorder of the brain-gut axis, a construct describing a bidirectional interaction between the gastrointestinal tract (GIT), incorporating the intestinal epithelial barrier, the mucosa-associated lymphoid tissue (MALT), gut muscle and the enteric nervous system (ENS), and the central nervous system (CNS) ( 9, 10 ). Most recently, the proposal that low-grade infl ammation, as evidenced by the release of mast cell mediators and activation of lymphocytes in the colo-rectal mucosa and by the detection of elevated levels of pro-infl ammatory cytokines in serum ( 8,(11)(12)(13), has provided a new dimension to this paradigm. The source of this low-grade infl ammation, or immune activation, whether luminal or central, has remained elusive. Polyunsaturated fatty acids (PUFA) and their metabolites have been shown to infl uence infl ammatory processes ( 14 ). Moreover, a pro-infl ammatory PUFA profi le has recently been reported in the maternal separation rodent model, an animal model of IBS ( 15 ).Abstract Irritable bowel syndrome (IBS) is the most common functional gastrointestinal disorder referred to gastroenterologists. Although the pathophysiology remains unclear, accumulating evidence points to the presence of low-level immune activation both in the gut and systemically. Circulating polyunsaturated fatty acids (PUFA) have recently attracted attention as being altered in a variety of disease states. Arachidonic acid (AA), in particular, has been implicated in the development of a pro-infl ammatory profi le in a number of immune-related disorders. AA is the precursor of a number of important immunomodulatory eicosanoids, including prostaglandin E 2 (PGE 2 ) and leukotriene B 4 (LTB 4 ). We investigated the hypothesis that elevated plasma AA concentrations in plasma contribute to the proposed pro-infl ammatory profi le in IBS. Plasma AA and related PUFA were quantifi ed by gas chromatography analysis in IBS patients and controls. Both PGE 2 and LTB 4 were measured in serum using commercially available ELISA assays. AA concentrations were elevated in our patient cohort compared with healthy controls. Moreover, we demonstrated that this disturbance in plasma AA concentrations leads to downstream elevations in eicosanoids. Together, our data identifi es...

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“…Guerreiro et al (2009) examined the role of the IL-6 À174G/C SNP, fat intake and the risk of developing Crohn's disease. Individuals homozygous for the C allele had a sixfold higher risk for Crohn's disease.…”

Section: Il-6 and Dietary Fasmentioning

confidence: 99%

Fatty acid–gene interactions, adipokines and obesity

Stryjecki

Mutch

2011

Eur J Clin Nutr

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It is now recognized that the low-grade inflammation observed with obesity is associated with the development of a wide range of downstream complications. As such, there is considerable interest in elucidating the regulatory mechanisms underlying the production of inflammatory molecules to improve the prevention and treatment of obesity and its co-morbidities. White adipose tissue is no longer considered a passive reservoir for storing lipids, but rather an important organ influencing energy metabolism, insulin sensitivity and inflammation by the secretion of proteins, commonly referred to as adipokines. Dysregulation of several adipokines, such as tumor necrosis factor-alpha (TNF-a), interleukin-6 (IL-6) and adiponectin, contributes to the low-grade inflammation that is a hallmark of obesity. Evidence now suggests that fatty acids represent a class of molecules that can modulate adipokine production, thereby influencing inflammatory status. Although the precise molecular mechanisms by which dietary fats regulate adipokine production remain unclear, recent findings indicate that diet-gene interactions may have an important role in the transcriptional and secretory regulation of adipokines. Single-nucleotide polymorphisms in the genes encoding TNF-a, IL-6 and adiponectin can modify circulating levels of these adipokines and, subsequently, obesity-related phenotypes. This genetic variation can also alter the influence of dietary fatty acids on adipokine production. Therefore, the current review will show that it is paramount to consider both genetic information and dietary fat intake to unravel the interindividual variability in inflammatory response observed in intervention protocols targeting obesity.

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Fatty Acids, IL6 and TNFα Polymorphisms: An Example of Nutrigenetics in Crohn's Disease

Cited by 56 publications

References 30 publications

Risk factors for metabolic bone disease in Crohnʼs disease patients

Risk factors for metabolic bone disease in Crohnʼs disease patients

Marked elevations in pro-inflammatory polyunsaturated fatty acid metabolites in females with irritable bowel syndrome

Fatty acid–gene interactions, adipokines and obesity

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