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Friday, 17 April 2015

Alaskan seaweeds lower inflammation in RAW 264.7 macrophages and decrease lipid accumulation in 3T3-L1 adipocytes

Volume 15, May 2015, Pages 396–407

Alaskan seaweeds lower inflammation in RAW 264.7 macrophages and decrease lipid accumulation in 3T3-L1 adipocytes

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Highlights

3 species of brown seaweed significantly inhibited 5 macrophage inflammatory genes.
Fractions of Fucus distichus decrease lipid accumulation in 3T3-L1 adipocytes.
F. distichus elevates expression of metabolic regulators in adipocytes.
F. distichus contains bioactive high molecular-weight fucophlorethol phlorotannins.
A bioactive monoglycosyldiacylglycerol (MGDG) was isolated form F. distichus.

Abstract

Chronic inflammation is characterized by macrophage accumulation in adipose tissue, which subsequently up-regulates pro-inflammatory cytokines and promotes the dysregulation of lipid metabolism, ultimately leading to insulin resistance. This study was designed to examine the effects of coastal Alaskan seaweeds on the macrophage inflammatory response and lipid metabolism of adipocytes. Two bioactive subfractions from the brown alga Fucus distichus, a monoglycosyldiacylglycerol subfraction and a phlorotannin subfraction, decreased mRNA expression of acute and chronic inflammatory biomarkers. Expression of Toll-like receptors TLR4 and TLR9 were also reduced, suggesting a potential mechanism of anti-inflammatory activity via TLR attenuation. F. distichus fractions decreased lipid accumulation up to 55% and increased free glycerol concentrations by 28–45%. This result was supported by increases in adiponectin and UCP-1 and decreases in leptin mRNA expression. Overall, the Alaskan seaweed F. distichus inhibited proinflammatory responses and improved lipid metabolism, suggesting the potential for seaweed phytochemicals to attenuate inflammatory diseases.

Keywords

  • Seaweed;
  • Phlorotannin;
  • Monoglycosyldiacylglycerol;
  • Inflammation;
  • Insulin resistance;
  • Fucus distichus

Corresponding author. 600 Laureate Way, Kannapolis, NC 28081. Tel.: +1 704 250 5407; fax: +1 704 250 5409.