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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2024.2
- 수록면
- 92 - 97 (6page)
- DOI
- https://doi.org/10.5483/BMBRep.2023-0158
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초록· 키워드
오류제보하기
Elevated blood glucose is associated with an increased risk ofatherosclerosis. Data from the current study showed that gluco samine (GlcN), a normal glucose metabolite of the hexosaminebiosynthetic pathway (HBP), promoted lipid accumulation inRAW264.7 macrophage cells. Oleic acid- and lipopolysaccha ride (LPS)-induced lipid accumulation was further enhanced byGlcN in RAW264.7 cells, although there was no a significantchange in the rate of fatty acid uptake. GlcN increased acetylCoA carboxylase (ACC), fatty acid synthase (FAS), scavenger re ceptor class A, liver X receptor, and sterol regulatory element binding protein-1c (SREBP-1c) mRNA expression, and; converse ly, suppressed ATP-binding cassette transporter A1 (ABCA-1) andABCG-1 expression. Additionally, GlcN promoted O-GlcNAcy lation of nuclear SREBP-1 but did not affect its DNA bindingactivity. GlcN stimulated phosphorylation of mammalian targetof rapamycin (mTOR) and S6 kinase. Rapamycin, a mTOR-spe cific inhibitor, suppressed GlcN-induced lipid accumulation inRAW264.7 cells. The GlcN-mediated increase in ACC and FASmRNA was suppressed, while the decrease in ABCA-1 andABCG-1 by GlcN was not significantly altered by rapamycin. To gether, our results highlight the importance of the mTOR signal ing pathway in GlcN-induced macrophage lipid accumulationand further support a potential link between mTOR and HBPsignaling in lipogenesis.
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