Anti-Inflammatory Effects of L-Fucose in 3T3-L1 Adipocytes

L-fucose is a monosaccharide derived from brown algae and has potential applications as a functional food ingredient. Previous studies have reported that L-fucose reduces lipid accumulation in murine adipose tissue. Adipose tissue not only regulates energy metabolism but also functions as an endocrine organ involved in inflammation through the production and secretion of various adipokines. L-fucose is expected to exert anti-inflammatory effects and modulate adipokine secretion in adipocytes. In the present study, we investigated the anti-inflammatory effects of L-fucose in adipocytes. L-fucose significantly suppressed the expression of pro-inflammatory mediators and reduced the production of reactive oxygen species induced by inflammatory stimulation with a combination of lipopolysaccharide (LPS), tumor necrosis factor-⍺ (TNF-⍺), and interferon-γ (IFN-γ). These effects are likely mediated through the inhibition of key signaling pathways, including mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) pathways. Additionally, we found that L-fucose promoted the multimerization and secretion of high molecular weight (HMW) adiponectin, even under inflammatory conditions. Our results suggest that although L-fucose downregulates adiponectin expression, it contributes to the formation and/or stabilization of HMW adiponectin, which is functionally more relevant in anti-inflammatory and metabolic regulation. L-fucose thus holds promise as a functional food ingredient for mitigating inflammation in adipocytes.

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Journal
Obesities
Published
2025-10-11
DOI
https://doi.org/10.3390/obesities5040074
Primary Topic
Adipokines, Inflammation, and Metabolic Diseases
Type
article
Field-Weighted Citation Impact
0.00

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article

Anti-Inflammatory Effects of L-Fucose in 3T3-L1 Adipocytes

Yuri Kominami, Hideki Ushio, Tomohiko Nakao, Teruki Aizawa et al.
Obesities
Adipokines, Inflammation, and Metabolic Diseases
article

Anti-Inflammatory Effects of L-Fucose in 3T3-L1 Adipocytes

Yuri Kominami, Hideki Ushio, Tomohiko Nakao, Teruki Aizawa, Yusuke Akahori, Tomoya Nakamura, Kazuki Mochizuki, Kazuyuki Ohara, Miho Ito, Tomoya Ueno
article en

Abstract

L-fucose is a monosaccharide derived from brown algae and has potential applications as a functional food ingredient. Previous studies have reported that L-fucose reduces lipid accumulation in murine adipose tissue. Adipose tissue not only regulates energy metabolism but also functions as an endocrine organ involved in inflammation through the production and secretion of various adipokines. L-fucose is expected to exert anti-inflammatory effects and modulate adipokine secretion in adipocytes. In the present study, we investigated the anti-inflammatory effects of L-fucose in adipocytes. L-fucose significantly suppressed the expression of pro-inflammatory mediators and reduced the production of reactive oxygen species induced by inflammatory stimulation with a combination of lipopolysaccharide (LPS), tumor necrosis factor-⍺ (TNF-⍺), and interferon-γ (IFN-γ). These effects are likely mediated through the inhibition of key signaling pathways, including mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) pathways. Additionally, we found that L-fucose promoted the multimerization and secretion of high molecular weight (HMW) adiponectin, even under inflammatory conditions. Our results suggest that although L-fucose downregulates adiponectin expression, it contributes to the formation and/or stabilization of HMW adiponectin, which is functionally more relevant in anti-inflammatory and metabolic regulation. L-fucose thus holds promise as a functional food ingredient for mitigating inflammation in adipocytes.

ObesitiesVol. 5(4)
Suzuki (Japan) (JP), The University of Tokyo (JP)
Google, Japan Society for the Promotion of Science
Openalex Percentile: Top 61%
Adipokines, Inflammation, and Metabolic Diseases
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Anti-Inflammatory Effects of L-Fucose in 3T3-L1 Adipocytes — Yuri Kominami, Hideki Ushio, et al. · Obesities (2025) | TGRS Research Map | TGRS