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.