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

Abstract 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...

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Autores principales:	Chanawee Jakkawanpitak, Masashi Inafuku, Hirosuke Oku, Nongporn Hutadilok-Towatana, Ruthaiwan Bunkrongcheap, Natthawan Sermwittayawong, Piyapat Aiemchareon, Decha Sermwittayawong
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/273807862f85410ebe705ca2ec7f3248
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spelling	oai:doaj.org-article:273807862f85410ebe705ca2ec7f32482021-12-02T18:48:23ZMechanism of the fungal-like particles in the inhibition of adipogenesis in 3T3-L1 adipocytes10.1038/s41598-021-98385-y2045-2322https://doaj.org/article/273807862f85410ebe705ca2ec7f32482021-09-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-98385-yhttps://doaj.org/toc/2045-2322Abstract 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.Chanawee JakkawanpitakMasashi InafukuHirosuke OkuNongporn Hutadilok-TowatanaRuthaiwan BunkrongcheapNatthawan SermwittayawongPiyapat AiemchareonDecha SermwittayawongNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-18 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Chanawee Jakkawanpitak Masashi Inafuku Hirosuke Oku Nongporn Hutadilok-Towatana Ruthaiwan Bunkrongcheap Natthawan Sermwittayawong Piyapat Aiemchareon Decha Sermwittayawong Mechanism of the fungal-like particles in the inhibition of adipogenesis in 3T3-L1 adipocytes
description	Abstract 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.
format	article
author	Chanawee Jakkawanpitak Masashi Inafuku Hirosuke Oku Nongporn Hutadilok-Towatana Ruthaiwan Bunkrongcheap Natthawan Sermwittayawong Piyapat Aiemchareon Decha Sermwittayawong
author_facet	Chanawee Jakkawanpitak Masashi Inafuku Hirosuke Oku Nongporn Hutadilok-Towatana Ruthaiwan Bunkrongcheap Natthawan Sermwittayawong Piyapat Aiemchareon Decha Sermwittayawong
author_sort	Chanawee Jakkawanpitak
title	Mechanism of the fungal-like particles in the inhibition of adipogenesis in 3T3-L1 adipocytes
title_short	Mechanism of the fungal-like particles in the inhibition of adipogenesis in 3T3-L1 adipocytes
title_full	Mechanism of the fungal-like particles in the inhibition of adipogenesis in 3T3-L1 adipocytes
title_fullStr	Mechanism of the fungal-like particles in the inhibition of adipogenesis in 3T3-L1 adipocytes
title_full_unstemmed	Mechanism of the fungal-like particles in the inhibition of adipogenesis in 3T3-L1 adipocytes
title_sort	mechanism of the fungal-like particles in the inhibition of adipogenesis in 3t3-l1 adipocytes
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/273807862f85410ebe705ca2ec7f3248
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Mechanism of the fungal-like particles in the inhibition of adipogenesis in 3T3-L1 adipocytes

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