Dietary Linoleic Acid Lowering Reduces Lipopolysaccharide-Induced Increase in Brain Arachidonic Acid Metabolism

Taha, Ameer Y.; Blanchard, H.; Cheon, Yewon; Ramadan, Epolia; Chen, Mei; Chang, Lisa; Rapoport, Stanley I.

doi:10.1007/s12035-016-9968-1

Cited by 42 publications

(32 citation statements)

References 64 publications

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“…In response to LPS, n-3 LC-PUFA-supplemented mice display an anti-inflammatory SPM profile whereas n-3 LC-PUFA-deficient mice exhibit a pro-inflammatory SPM profile [69]. These results corroborate previous ones in vivo [171][172][173][174][175][176] and in vitro in macrophages [177,178] and microglia [179][180][181].…”

Section: Nutrition As a Factor Of Variation Of Spm Levelssupporting

confidence: 86%

Polyunsaturated Fatty Acid Metabolism in the Brain and Brain Cells

Joffre¹

2019

Feed Your Mind - How Does Nutrition Modulate Brain Function Throughout Life?

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Dietary polyunsaturated fatty acids (PUFAs) have gained more importance these last decades since they regulate the level of long-chain PUFAs (LC-PUFAs) in all cells and especially in brain cells. Because LC-PUFAs, especially those of the n-3 family, display both anti-inflammatory and pro-resolution properties, they play an essential role in neuroinflammation. Neuroinflammation is a hallmark of neurological disorders and requires to be tightly controlled or at least limited otherwise it can have functional consequences and negatively impact the quality of life and well-being of patients. LC-PUFAs exert these beneficial properties in part through the synthesis of specialized pro-resolving mediators (SPMs) that are involved in the resolution of inflammation and to the return of homeostasis. SPMs are promising relevant candidates to resolve brain inflammation and to contribute to neuroprotective functions and lead to novel therapeutics for brain inflammatory diseases. Here we present an overview of the origin and accumulation of PUFAs in the brain and brain cells and their conversion into SPMs that are involved in neuroinflammation and how nutrition induces variations in LC-PUFA and SPM levels in the brain and in brain cells.

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Section: Nutrition As a Factor Of Variation Of Spm Levelssupporting

confidence: 86%

Polyunsaturated Fatty Acid Metabolism in the Brain and Brain Cells

Joffre¹

2019

Feed Your Mind - How Does Nutrition Modulate Brain Function Throughout Life?

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“…Because only extreme differences in LA intake have previously been documented to alter a small number of tissue AA oxylipins (4,14,15,33), and because there is strong evidence that dietary LA does not alter blood AA levels (16), it has been concluded that dietary LA has minimal effects on AA oxylipins. The current findings, however, demonstrate that increased dietary LA within the usual dietary range resulted in higher levels of 10-12 AA oxylipins in kidney and liver, as well as many LA, GLA, EDA, DGLA, and AdA oxylipins in these tissues, and LA oxylipins in serum.…”

Section: Discussionmentioning

confidence: 99%

“…These oxygenated because a higher n-6/n-3 PUFA ratio is thought to increase inflammation via its effect on altering the n-6/n-3 oxylipin profile (11)(12)(13). However, although it has recently been shown that large changes in LA alter the levels of LA oxylipins (4,14,15), whether changes in dietary LA in the normal range of current intake affect LA oxylipins is not known. The effect of dietary LA on LA oxylipins is also likely important because LA oxylipins can make up more than half of all oxylipins by mass (e.g., rat kidney) (4).…”

mentioning

confidence: 99%

Dietary LA and sex effects on oxylipin profiles in rat kidney, liver, and serum differ from their effects on PUFAs

Leng

Winter

Aukema

2017

Journal of Lipid Research

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A vast literature on fatty acids in mammals exists, but comparable compositional data on oxylipins is lacking. Weanling Sprague-Dawley rats were therefore provided control diets or diets with higher linoleic acid (LA) or with higher LA and α-linolenic acid (LA+ALA) for 6 weeks. Kidneys, livers, and serum were analyzed for oxylipins and fatty acids. The proportion of tissue oxylipins derived from LA was greater than the relative proportion of LA itself, whereas arachidonic acid (AA) oxylipins were overrepresented in serum. Higher dietary LA increased kidney LA and AA oxylipins, despite not altering LA or AA. In liver, both LA and AA and their oxylipins were higher, whereas in serum only LA oxylipins were higher with higher dietary LA. Higher LA resulted in a higher ratio of n-6/n-3 PUFA-derived oxylipins; adding ALA to the LA diet mitigated this and many, but not all, effects of the LA diet. Approximately 40% of oxylipins detected were influenced by sex and, unlike their PUFA precursors, most (>90%) of these were higher in males. These differences in dietary LA and sex on oxylipin and fatty acid profiles further our understanding of the effects of fatty acids and may have implications for dietary LA recommendations.

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“…Recent work highlighted that dietary supplementation with n-3 PUFAs and antioxidants dramatically increases Ab phagocytosis by monocytes (Fiala et al, 2015). As discussed before, increasing DHA levels via dietary means or genetic approaches potently reduces brain proinflammatory cytokine production in animal models of acute and chronic inflammation (Orr et al, 2013;Delpech et al, 2015a,b;Taha et al, 2017), aging (Labrousse et al, 2012;Moranis et al, 2012), or AD (Casali et al, 2015;Hopperton et al, 2016). Concomitantly, DHA potently promotes microglia phagocytic activity (Chen et al, 2014), including toward Ab in vitro (Hjorth et al, 2013).…”

Section: A Lc-pufa Dietary Interventions To Limit Neuroinflammationmentioning

confidence: 98%

Anti-Inflammatory Effects of Omega-3 Fatty Acids in the Brain: Physiological Mechanisms and Relevance to Pharmacology

Layé¹,

Nadjar²,

Joffre³

et al. 2017

Pharmacol Rev

324

190

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Classically, polyunsaturated fatty acids (PUFA) were largely thought to be relatively inert structural components of brain, largely important for the formation of cellular membranes. Over the past 10 years, a host of bioactive lipid mediators that are enzymatically derived from arachidonic acid, the main n-6 PUFA, and docosahexaenoic acid, the main n-3 PUFA in the brain, known to regulate peripheral immune function, have been detected in the brain and shown to regulate microglia activation. Recent advances have focused on how PUFA regulate the molecular signaling of microglia, especially in the context of neuroinflammation and behavior. Several active drugs regulate brain lipid signaling and provide proof of concept for targeting the brain. Because brain lipid metabolism relies on a complex integration of diet, peripheral metabolism, including the liver and blood, which supply the brain with PUFAs that can be altered by genetics, sex, and aging, there are many pathways that can be disrupted, leading to altered brain lipid homeostasis. Brain lipid signaling pathways are altered in neurologic disorders and may be viable targets for the development of novel therapeutics. In this study, we discuss in particular how n-3 PUFAs and their metabolites regulate microglia phenotype and function to exert their anti-inflammatory and proresolving activities in the brain.

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Dietary Linoleic Acid Lowering Reduces Lipopolysaccharide-Induced Increase in Brain Arachidonic Acid Metabolism

Cited by 42 publications

References 64 publications

Polyunsaturated Fatty Acid Metabolism in the Brain and Brain Cells

Polyunsaturated Fatty Acid Metabolism in the Brain and Brain Cells

Dietary LA and sex effects on oxylipin profiles in rat kidney, liver, and serum differ from their effects on PUFAs

Anti-Inflammatory Effects of Omega-3 Fatty Acids in the Brain: Physiological Mechanisms and Relevance to Pharmacology

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