What is the clinical evidence from this study?

Study design: Other. Population: Obesity-induced adipose tissue inflammation. Intervention: Docosahexaenoic acid (DHA) and Resolvin D1.

What question did this study set out to answer?

To elucidate the cellular and molecular mechanisms through which docosahexaenoic acid (DHA) and its pro-resolving metabolite resolvin D1 alleviate adipose tissue inflammation in obesity.

October 18, 2011The Journal of Immunology

Resolvin D1 and Its Precursor Docosahexaenoic Acid Promote Resolution of Adipose Tissue Inflammation by Eliciting Macrophage Polarization toward an M2-Like Phenotype

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Key result

Docosahexaenoic acid (4 μg/g) and resolvin D1 reduced proinflammatory Th1 cytokines and promoted a phenotypic switch toward an M2-like macrophage phenotype in adipose tissue of obese mice.

Population

High-fat diet-induced obese mice and their adipose tissue, adipocytes, and stromal vascular cells (SVC)

Design

Preclinical

Authors

ETEsther TitosHospital Clínic de Barcelona BRBibiana RiusScripps Institution of Oceanography AGAna González‐PérizHospital Clínic de Barcelona

Discussion

Member takes

Implication

Should not change clinical practice; hypothesis-generating for DHA/resolvin D1 in human obesity inflammation.

Key Points

To elucidate the cellular and molecular mechanisms through which docosahexaenoic acid (DHA) and its pro-resolving metabolite resolvin D1 alleviate adipose tissue inflammation in obesity.
Treated high-fat diet-induced obese mice with DHA (4 μg/g) to evaluate macrophage markers, cytokine secretion, and adipocyte morphology in adipose tissue.
Treated adipose tissue stromal vascular cells (SVC) in vitro with resolvin D1 under IFN-γ/LPS stimulation to assess cytokine production, arginase 1 expression, phagocytosis, and reactive oxygen species generation.
DHA treatment reduced high CD11b/high F4/80-expressing macrophages and upregulated M2 markers (IL-10, CD206, arginase 1, resistin-like molecule α, chitinase-3 like protein) while inhibiting Th1 cytokine secretion (IL-6, MCP-1, TNF-α) in adipose stromal vascular cells.
Resolvin D1 concentration-dependently suppressed IFN-γ/LPS-induced Th1 cytokines, upregulated arginase 1, decreased reactive oxygen species, and enhanced nonphlogistic phagocytosis in adipose macrophages without affecting adipocyte area or hormone-sensitive lipase phosphorylation.

Structured PICO

Population

High-fat diet-induced obese mice used to study the mechanisms of omega-3 polyunsaturated fatty acids on adipose tissue inflammation.

Intervention

Docosahexaenoic acid (DHA; 4 μg/g) and resolvin D1

Outcome

Macrophage polarization toward an M2-like phenotype and expression of inflammatory cytokinessurrogate

DHA and its metabolite resolvin D1 promote the resolution of obesity-induced adipose tissue inflammation by shifting macrophages toward an anti-inflammatory M2-like phenotype.

Cite This Study

Titos et al. (2011) studied Obesity-induced adipose tissue inflammation. Docosahexaenoic acid (DHA) and Resolvin D1 was evaluated. Docosahexaenoic acid (4 μg/g) and resolvin D1 reduced proinflammatory Th1 cytokines and promoted a phenotypic switch toward an M2-like macrophage phenotype in adipose tissue of obese mice.

synapsesocial.com/papers/6a7307bd91c366bb2031e558 https://doi.org/10.4049/jimmunol.1100225

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Resolvin D1 and Its Precursor Docosahexaenoic Acid Promote Resolution of Adipose Tissue Inflammation by Eliciting Macrophage Polarization toward an M2-Like Phenotype

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Resolvin D1 and Its Precursor Docosahexaenoic Acid Promote Resolution of Adipose Tissue Inflammation by Eliciting Macrophage Polarization toward an M2-Like Phenotype

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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