Elsevier

Advances in Nutrition

Volume 2, Issue 4, July 2011, Pages 304-316
Advances in Nutrition

(n-3) Fatty Acids Alleviate Adipose Tissue Inflammation and Insulin Resistance: Mechanistic Insights

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ABSTRACT

Obesity is associated with the metabolic syndrome, a significant risk factor for developing type 2 diabetes and cardiovascular diseases. Chronic low-grade inflammation occurring in the adipose tissue of obese individuals is causally linked to the pathogenesis of insulin resistance and the metabolic syndrome. Although the exact trigger of this inflammatory process is unknown, adipose tissue hypoxia, endoplasmic reticular stress, and saturated fatty acid–mediated activation of innate immune processes have been identified as important processes in these disorders. Furthermore, macrophages and T lymphocytes have important roles in orchestrating this immune process. Although energy restriction leading to weight loss is the primary dietary intervention to reverse these obesity-associated metabolic disorders, other interventions targeted at alleviating adipose tissue inflammation have not been explored in detail. In this regard, (n-3) PUFA of marine origin both prevent and reverse high-fat-diet–induced adipose tissue inflammation and insulin resistance in rodents. We provide an update on the pathogenesis of adipose tissue inflammation and insulin resistance in obesity and discuss potential mechanisms by which (n-3) PUFA prevent and reverse these changes and the implications in human health.

Abbreviations used

AA
arachidonic acid
ALA
α-linolenic acid
AMPK
AMP-activated protein kinase
ATM
adipose tissue macrophage
Ccr
C-C motif chemokine receptor
CD
cluster of differentiation
ECM
extracellular matrix
ER
endoplasmic reticulum
GPR
G protein–coupled receptor
IRS
insulin receptor substrate
JNK
jun N-terminal kinase
LA
linoleic acid
M1
classically activated macrophage
M2
alternatively activated macrophage
MCP
monocyte chemotactic protein
MGL
macrophage galactose N-acetyl-galactosamine specific lectin
PAI
plasminogen activator inhibitor
PI3K
phosphatidylinositol 3-kinase
PSGL
P-selectin glycoprotein ligand
SOCS
suppressor of cytokine signaling
TAK
TGF-βactivated kinase
Th
helper T cell
TLR
Toll-like receptor

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Supported by a National Institute of Food and Agriculture-National Research Initiative award (2005-35200-15224), an AHA Southeast Affiliate Predoctoral Fellowship, the University of Tennessee (UT) Obesity Research Center, UT AgResearch, and UT Extension.

Author disclosures: N. S. Kalupahana, K. J. Claycombe, and N. Moustaid-Moussa, no conflicts of interest.