Unsaturated fatty acids repress the expression of adipocyte fatty acid binding protein via the modulation of histone deacetylation in RAW 264.7 macrophages

Coleman, Sara L.; Park, Youngki; Lee, Ji-Young

doi:10.1007/s00394-010-0140-9

Cited by 18 publications

(13 citation statements)

References 48 publications

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“…This study revealed that mobilization of bioactive lipids from adipose tissue regulates systemic metabolic homeostasis. Other works have confirmed that increased palmitoleate production influences metabolism in the absence of FABP and through activation of SCD1 (65,66).…”

Section: Is Palmitoleate a Lipokine?mentioning

confidence: 80%

The Role of the Novel Lipokine Palmitoleic Acid in Health and Disease

Frigolet

Gutiérrez-Aguilar

2017

Advances in Nutrition

197

143

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The monounsaturated fatty acid palmitoleate (palmitoleic acid) is one of the most abundant fatty acids in serum and tissues, particularly adipose tissue and liver. Its endogenous production by stearoyl-CoA desaturase 1 gives rise to its cis isoform, cis-palmitoleate. Although trans-palmitoleate is also synthesized in humans, it is mainly found as an exogenous source in ruminant fat and dairy products. Recently, palmitoleate was considered to be a lipokine based on evidence demonstrating its release from adipose tissue and its metabolic effects on distant organs. After this finding, research has been performed to determine whether palmitoleate has beneficial effects on metabolism and to elucidate the underlying mechanisms. Thus, the aim of this work was to review the current status of knowledge about palmitoleate, its metabolism, and its influence on metabolic abnormalities. Results have shown mixed cardiovascular effects, direct or inverse correlations with obesity, and hepatosteatosis, but a significant amelioration or prevention of insulin resistance and diabetes. Finally, the induction of palmitoleate release from adipose tissue, dietary intake, and its supplementation are all interventions with a potential impact on certain metabolic diseases. Adv Nutr 2017;8(Suppl):173S-81S.

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Section: Is Palmitoleate a Lipokine?mentioning

confidence: 80%

The Role of the Novel Lipokine Palmitoleic Acid in Health and Disease

Frigolet

Gutiérrez-Aguilar

2017

Advances in Nutrition

197

143

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“…Dendritic cells deficient in FABPs were poor producers of pro-inflammatory cytokines-interleukin-6 (IL-6) and TNF-α- and did not promote pro-inflammatory T-cell responses, suggesting that metabolic-inflammatory pathway cross-regulation by A-FABPs plays a significant role in adaptive immune responses and inflammation [10]. These results-coupled with the observations that unsaturated fatty acids, such as palmitoleic acid, oleic acid, linoleic acid, linolenic acid, and eicosapentaenoic acid, significantly repressed the basal as well as lipopolysaccharide-induced A-FABP expression in macrophages and depletion of A-FABP expression by RNA interference (RNAi) decreased cyclooxygenase 2 (COX-2) mRNA expression and potentiated the repression by linoleic acid [11] -give interesting insights into the relationship among A-FABP, cytokines, and unsaturated fatty acids and their involvement in sepsis and other critical illnesses.…”

Section: Adipose-fatty Acid-binding Protein and Inflammationmentioning

confidence: 97%

Serum adipocyte fatty acid-binding protein in the critically ill

Das

2013

Critical Care

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Sepsis due to unabated inflammation is common. Increased production of pro-inflammatory cytokines, free radicals, and eicosanoids has been detected in sepsis and other critical illnesses but could also be due to decreased synthesis and release of anti-inflammatory molecules. Increased serum adipose-fatty acid-binding protein (A-FABP) levels can cause insulin resistance and have been reported in the critically ill, serve as a marker of prognosis, and thus link metabolic homeostasis and inflammation. A-FABP can be linked to the expression of Toll-like receptors, macrophage activation, synthesis and release of pro-inflammatory cytokines interleukin-6 and tumor necrosis factor-alpha, activation of cyclooxygenase 2 (COX-2) expression, and eicosanoid synthesis, events that can cause insulin resistance and initiation and progression of inflammation and sepsis. Unsaturated fatty acids and their anti-inflammatory products, such as lipoxins, resolvins, and protectins, may suppress A-FABP expression, inhibit macrophage and COX-2 activation, and decrease production of pro-inflammatory cytokines and ultimately could lead to a decrease in insulin resistance and resolution of inflammation and recovery from sepsis. Serial measurement of these pro- and anti-inflammatory molecules and correlation of their levels to the progression to or recovery from (or both) sepsis and other inflammatory processes may form a new approach to predict prognosis in inflammatory conditions and eventually could lead to the development of new therapeutic strategies.

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“…What is more, unsaturated fatty acids often counteract inflammatory pathways induced by saturated fatty acids; for example, in macrophages PUFAs suppress palmitic acid-induced increases in LOX1 and FABP expression [66;67]. Conjugated linoleic acid (CLA) has been shown to cause regression of preestablished murine atherosclerotic plaques, accompanied by a decrease in lesion macrophage accumulation and suppressed COX2, cPLA2, MCP1, and MMP9 expression in macrophages [68].…”

Section: Macrophage Phenotypic Polarization In Response To Anti-inflamentioning

confidence: 99%

Phenotypic modulation of macrophages in response to plaque lipids

Adamson

Leitinger

2011

Current Opinion in Lipidology

130

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Purpose of review The accumulation of macrophages in the vascular wall is a hallmark of atherosclerosis. The biological properties of atherosclerotic plaque macrophages determine lesion size, composition and stability. In atherosclerotic plaques, macrophages encounter a microenvironment that is comprised of a variety of lipid oxidation products, each of which has diverse biological effects. In this review, we summarize recent advances in our understanding of the effects of plaque lipids on macrophage phenotypic polarization. Recent findings Atherosclerotic lesions in mice and in humans contain various macrophage phenotypes, which play different roles in mediating inflammation, the clearance of dead cells, and possibly resolution. Macrophages alter their phenotype and biological function in response to plaque lipids through the upregulation of specific sets of genes. Interaction of oxidized lipids with pattern recognition receptors and activation of the inflammasome by cholesterol crystals drive macrophages towards an inflammatory M1 phenotype. A new phenotype, Mox, develops when oxidized phospholipids activate stress response genes via Nrf2. Other lipid mediators such as nitrosylated-fatty acids and omega-3 fatty acid-derived products polarize plaque macrophages towards anti-inflammatory and proresolving phenotypes. Summary A deeper understanding of how lipids that accumulate in atherosclerotic plaques affect macrophage phenotype and function and thus atherosclerotic lesion development and stability will help to devise novel strategies for intervention.

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Unsaturated fatty acids repress the expression of adipocyte fatty acid binding protein via the modulation of histone deacetylation in RAW 264.7 macrophages

Cited by 18 publications

References 48 publications

The Role of the Novel Lipokine Palmitoleic Acid in Health and Disease

The Role of the Novel Lipokine Palmitoleic Acid in Health and Disease

Serum adipocyte fatty acid-binding protein in the critically ill

Phenotypic modulation of macrophages in response to plaque lipids

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