β-Glucan from Aureobasidum species inhibits fat accumulation in 3T3-L1 adipocyte differentiation

Kim, Mi‐Ja; Kim, Ork-Hee; Cheong, Chul; Jang, Ki‐Hyo; Kim, Chul‐Ho; Kang, Soon Ah

doi:10.1007/s10068-015-0146-4

Cited by 3 publications

(2 citation statements)

References 14 publications

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“…Similarly, bacterial β-glucan from Aureobasidium sp. inhibited adipogenesis in 3T3-L1 adipocytes by decreasing the expression of PPARγ, acetyl-CoA carboxylase (ACC), and FABP4 (aP2) genes [ 33 ]. Based on the quantitative RT-PCR results, the β-glucan-FBR extracts strongly inhibited adipogenesis in 3T3-L1 adipocytes.…”

Section: Resultsmentioning

confidence: 99%

Effect of Solid-State Fermented Brown Rice Extracts on 3T3-L1 Adipocyte Differentiation

Hun

2023

J. Microbiol. Biotechnol.

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Aspergillus oryzae KCCM 11372 was used to enhance the production of β-glucan using humidity control strategies. Under conditions of 60% humidity, solid-state fermentation (SSF) increased the yields of enzymes (amylase and protease), fungal biomass (ergosterol), and β-glucan. The maximum concentrations obtained were 14800.58 U/g at 72 h, 1068.14 U/g at 120 h, 1.42 mg/g at 72 h, and 12.0% (w/w) at 72 h, respectively. Moreover, the β-glucan containing fermented brown rice (β-glucan-FBR) extracts at concentrations of 25–300 μg/ml was considered noncytotoxic to 3T3-L1 preadipocytes. We then studied the inhibitory effects of the extracts on fat droplet formation in 3T3-L1 cells. As a result, 300 μg/ml of β-glucan-FBR extracts showed a high inhibition of 38.88% in lipid accumulation. Further, these extracts inhibited adipogenesis in the 3T3-L1 adipocytes by decreasing the expression of C/EBPα, PPARγ, aP2, and GLUT4 genes.

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Section: Resultsmentioning

confidence: 99%

Effect of Solid-State Fermented Brown Rice Extracts on 3T3-L1 Adipocyte Differentiation

Hun

2023

J. Microbiol. Biotechnol.

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“…To combat against obesity, many research investigators have identi ed molecules or compounds that inhibit adipogenesis. Among those, b-glucan, a polymer of b-glucoses that link through b-(1®3) glycosidic bonds and found in the cell walls of yeast, fungi and some seaweeds, has been shown to inhibit adipogenesis [8][9][10] . Noticeably, a previous study demonstrated that yeast-derived insoluble β-1,3-glucan strongly inhibited adipogenesis better than soluble β-1,3-glucan 11 .…”

Section: Introductionmentioning

confidence: 99%

Mechanism of the Fungal-like Particles in the Inhibition of Adipogenesis in 3t3-l1 Adipocytes

Jakkawanpitak

Inafuku

Oku

et al. 2021

Preprint

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The dynamic ability of adipocytes in adipose tissue to store lipid in response to changes in the nutritional input and inflammatory elicitors has a major impact on human health. Previously, we established laminarin-coated beads or LCB as an inflammatory elicitor for adipocytes. However, it was not clear whether LCB inhibits lipid accumulation in adipocytes. Here, we show that LCB acts in the early stage of adipogenesis through both IRAK and SYK pathways, resulting in the activation of the AMPK and NF-kB complexes, which subsequently cause cell cycle arrest, suppression of C/EBPb, PPARg, C/EBPa, FAS, FABP4, and ACC proteins, downregulation of other transcription factors and enzymes, such as Pparg, C/ebpa, Srebp-1, Lpl, and Fas gene expression, inhibition of adipogenesis, and stimulation of an inflammatory response. Unlike the inhibition of adipogenesis, LCB could stimulate an inflammatory response at any stage of differentiation. In addition, we find that Tlr2 and Clec7a/Dectin-1 but not Tlr4 and Cd36 gene expression are upregulated upon the treatment with LCB, suggesting that TLR2 and CLEC7A/Dectin-1 might be the b-glucan receptors for the cells. Together, we present the mechanism of LCB, as fungal-like particles, that elicit an inflammatory response and inhibit adipogenesis at the early stage of differentiation.

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Mechanism of the fungal-like particles in the inhibition of adipogenesis in 3T3-L1 adipocytes

Jakkawanpitak

Inafuku

Oku

et al. 2021

Sci Rep

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The dynamic ability of adipocytes in adipose tissue to store lipid in response to changes in the nutritional input and inflammatory elicitors has a major impact on human health. Previously, we established laminarin-coated beads or LCB as an inflammatory elicitor for adipocytes. However, it was not clear whether LCB inhibits lipid accumulation in adipocytes. Here, we show that LCB acts in the early stage of adipogenesis through both interleukin-1 receptor-associated kinases (IRAK) and spleen tyrosine kinase (SYK) pathways, resulting in the activation of the AMP-activated protein kinase (AMPK) and nuclear factor-κB (NF-κB) complexes, which subsequently cause cell cycle arrest, downregulation of the key transcription factors and enzymes responsible for adipogenesis, inhibition of adipogenesis, and stimulation of an inflammatory response. While LCB could effectively block lipid accumulation during the early stage of adipogenesis, it could stimulate an inflammatory response at any stage of differentiation. Additionally, our results raise a possibility that toll-like receptor 2 (TLR2) and C-type lectin domain family 7 member A (CLEC7A/Dectin-1) might be potential β-glucan receptors on the fat cells. Together, we present the mechanism of LCB, as fungal-like particles, that elicits an inflammatory response and inhibits adipogenesis at the early stage of differentiation.

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β-Glucan from Aureobasidum species inhibits fat accumulation in 3T3-L1 adipocyte differentiation

Cited by 3 publications

References 14 publications

Effect of Solid-State Fermented Brown Rice Extracts on 3T3-L1 Adipocyte Differentiation

Effect of Solid-State Fermented Brown Rice Extracts on 3T3-L1 Adipocyte Differentiation

Mechanism of the Fungal-like Particles in the Inhibition of Adipogenesis in 3t3-l1 Adipocytes

Mechanism of the fungal-like particles in the inhibition of adipogenesis in 3T3-L1 adipocytes

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