• Macromolecular Research
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• v.16 no.1
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• pp.1-5
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• 2008

The enzymatic hydrolysis of chitin has been studied for almost a century, and early work established that at least two enzymes are required, a chitinase that mainly yields the disaccharide N,N'-diacetylchitobiose, or $(GlcNAc)_2$, and a "chitobiase", or ${\beta}$-N-acetylglucosaminidase, which gives the final product G1cNAc. This pathway has not been completely identified but has remained the central concept for the chitin catabolism through the $20^{th}$ century1 including in marine bacteria. However, the chitin catabolic cascade is quite complex, as described in this review. This report describes three biologically functional genes involved in the chitin catabolic cascade of Vibrios in an attempt to better understand the metabolic pathway of chitin.

• BMB Reports
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• v.57 no.2
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• pp.92-97
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• 2024

Elevated blood glucose is associated with an increased risk of atherosclerosis. Data from the current study showed that glucosamine (GlcN), a normal glucose metabolite of the hexosamine biosynthetic pathway (HBP), promoted lipid accumulation in RAW264.7 macrophage cells. Oleic acid- and lipopolysaccharide (LPS)-induced lipid accumulation was further enhanced by GlcN in RAW264.7 cells, although there was no a significant change in the rate of fatty acid uptake. GlcN increased acetyl CoA carboxylase (ACC), fatty acid synthase (FAS), scavenger receptor class A, liver X receptor, and sterol regulatory element-binding protein-1c (SREBP-1c) mRNA expression, and; conversely, suppressed ATP-binding cassette transporter A1 (ABCA-1) and ABCG-1 expression. Additionally, GlcN promoted O-GlcNAcylation of nuclear SREBP-1 but did not affect its DNA binding activity. GlcN stimulated phosphorylation of mammalian target of rapamycin (mTOR) and S6 kinase. Rapamycin, a mTOR-specific inhibitor, suppressed GlcN-induced lipid accumulation in RAW264.7 cells. The GlcN-mediated increase in ACC and FAS mRNA was suppressed, while the decrease in ABCA-1 and ABCG-1 by GlcN was not significantly altered by rapamycin. Together, our results highlight the importance of the mTOR signaling pathway in GlcN-induced macrophage lipid accumulation and further support a potential link between mTOR and HBP signaling in lipogenesis.