Interaction entre le fer et les oméga 3 ?

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Interaction between iron and omega-3 fatty acids metabolisms: where is the cross-link?
Magdalena Ogłuszka Critical Reviews in Food Science and Nutrition Volume 62, 2022 - Issue 11

Iron is an essential micronutrient for almost all living organisms. It plays an important role in DNA, RNA, and protein synthesis and takes part in electron transport, cellular respiration, cell proliferation and differentiation, and gene expression regulation. However, there is a fine line between excessive and insufficient body iron content. Iron overload is biochemically dangerous.

It causes serious toxicities and generates reactive oxygen species via the Fenton reaction, leading to damage to cellular membranes, proteins, and DNA. Omega-3 fatty acids play an essential role in many physiological processes, including energy metabolism and signal transduction, as well as acting as structural components of cell membranes. Omega-3 fatty acids also help to maintain homeostasis and combat diseases.

Recent studies using model organisms as well as clinical studies have revealed a link between omega-3 fatty acids and iron metabolism. Moreover, various iron-related disorders are significantly affected by omega-3 fatty acids. There is a clear relationship between iron and omega-3 fatty acid metabolisms; however, the underlying mechanisms are unknown. Therefore, in-depth research is needed to determine the exact nature of the metabolic interactions of these nutrients.

Here, we focus on iron and omega-3 fatty acid metabolisms at their crossroads in the liver and brain.

[Nutrimuscle-Conseils]

Healthy dietary intake moderates the effects of age on brain iron concentration and working memory performance
Valentinos Zachariou Neurobiology of Aging Volume 106, October 2021, Pages 183-196

Highlights
• Age-related brain iron accumulation is linked with cognitive decline.
• It remains unknown if nutrition can influence age-related increases in brain iron.
• Nutrients found in nuts/healthy oils/fish moderate age-related brain iron increases.
• These nutrients also moderate age-related declines in cognitive performance.

Age-related brain iron accumulation is linked with oxidative stress, neurodegeneration and cognitive decline. Certain nutrients can reduce brain iron concentration in animal models, however, this association is not well established in humans. Moreover, it remains unknown if nutrition can moderate the effects of age on brain iron concentration and/or cognition. Here, we explored these issues in a sample of 73 healthy older adults (61-86 years old), while controlling for several factors such as age, gender, years of education, physical fitness and alcohol-intake. Quantitative susceptibility mapping was used for assessment of brain iron concentration and participants performed an N-Back paradigm to evaluate working memory performance. Nutritional-intake was assessed via a validated questionnaire. Nutrients were grouped into nutrition factors based on previous literature and factor analysis.

One factor, comprised of vitamin E, lysine, DHA omega-3 and LA omega-6 PUFA, representing food groups such as nuts, healthy oils and fish, moderated the effects of age on both brain iron concentration and working memory performance, suggesting that these nutrients may slow the rate of brain iron accumulation and working memory declines in aging.

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Given established age-related reductions in combating oxidative stress with endogenous nonenzymatic antioxidants (e.g., glutathione, melatonin, vitamins A, C and E and flavonoids; Jovanovic 2014), increased intake of exogenous antioxidants (such as vitamin E and lysine) could become more important with increasing age.

[Nutrimuscle-Conseils]

High-dose ferric citrate supplementation attenuates omega-3 polyunsaturated fatty acid biosynthesis via downregulating delta 5 and 6 desaturases in rats with high-fat diet-induced obesity Food & Function Issue 23, 2021 Amelia Faradina

Obesity is associated with an increased risk of an iron deficiency; however, a synergistic relationship between iron and lipid homeostasis was also observed. The aim of this study was to investigate the effects of pharmacological doses of iron supplementation on omega 3 (n-3) and omega 6 (n-6) polyunsaturated fatty acids (PUFAs). Sprague-Dawley (SD) rats were fed a normal diet or a 50% high-fat diet (HFD) without or with pharmacological doses of ferric citrate (0.25, 1, or 2 g ferric iron per kg diet) for 12 weeks, and erythrocyte profiles of n-3 and n-6 PUFAs were quantitated. Ferric citrate supplementation showed dose-related effects on liver inflammation, liver iron accumulation, and increasing circulating levels of iron, erythrocyte degradation biomarkers LVV-hemorphin-7, malondialdehyde (MDA), and insulin.

Obese rats supplemented with 2 g ferric iron per kg diet also had decreased levels of eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and total n-3 PUFAs compared to rats fed a normal diet or HFD alone. A western blotting analysis revealed that iron-mediated downregulation of n-3 PUFA-converting enzymes (Δ5 and Δ6 desaturases) only occurred at high dosages (≥1 g ferric iron per kg diet). A Spearman correlation analysis showed that total liver iron and serum LVV-hemorphin-7 and MDA were negatively correlated with n-3 PUFAs and their converting enzymes (Δ5 and Δ6 desaturases) (all p < 0.05).

In conclusion, obese rats that received high-dose ferric citrate supplementation (>1 g of ferric iron per kg diet) exhibited decreased n-3 PUFA levels via downregulation of expressions of Δ5 and Δ6 desaturase enzymes.

[Nutrimuscle-Diététique]

Traduction de l'étude

Une supplémentation en citrate ferrique à haute dose atténue la biosynthèse des acides gras polyinsaturés oméga-3 en régulant à la baisse les delta 5 et 6 désaturases chez les rats souffrant d'obésité induite par un régime riche en graisses Food & Function Issue 23, 2021 Amelia Faradina

L'obésité est associée à un risque accru de carence en fer; cependant, une relation synergique entre l'homéostasie du fer et des lipides a également été observée. Le but de cette étude était d'étudier les effets de doses pharmacologiques de supplémentation en fer sur les acides gras polyinsaturés (AGPI) oméga 3 (n-3) et oméga 6 (n-6). Des rats Sprague-Dawley (SD) ont reçu une alimentation normale ou une alimentation riche en graisses (HFD) à 50 % sans ou avec des doses pharmacologiques de citrate ferrique (0,25, 1 ou 2 g de fer ferrique par kg d'alimentation) pendant 12 semaines, et les profils érythrocytaires des AGPI n-3 et n-6 ont été quantifiés. La supplémentation en citrate ferrique a montré des effets liés à la dose sur l'inflammation du foie, l'accumulation de fer dans le foie et l'augmentation des taux circulants de fer, les biomarqueurs de dégradation des érythrocytes LVV-hémorphine-7, le malondialdéhyde (MDA) et l'insuline.

Les rats obèses supplémentés avec 2 g de fer ferrique par kg de régime présentaient également une diminution des niveaux d'acide eicosapentaénoïque (EPA), d'acide docosapentaénoïque (DPA) et d'AGPI n-3 totaux par rapport aux rats nourris avec un régime normal ou HFD seul. Une analyse Western Blot a révélé que la régulation à la baisse médiée par le fer des enzymes de conversion des AGPI n-3 (désaturases Δ5 et Δ6) ne se produisait qu'à des doses élevées (≥ 1 g de fer ferrique par kg d'alimentation). Une analyse de corrélation de Spearman a montré que le fer hépatique total et le sérum LVV-hémorphine-7 et MDA étaient négativement corrélés avec les AGPI n-3 et leurs enzymes de conversion (Δ5 et Δ6 désaturases) (tous p < 0,05).

En conclusion, les rats obèses ayant reçu une supplémentation en citrate ferrique à forte dose (> 1 g de fer ferrique par kg de régime alimentaire) ont présenté une diminution des niveaux d'AGPI n-3 via une régulation à la baisse de l'expression des enzymes Δ5 et Δ6 désaturase.