PMID- 37964636
OWN - NLM
STAT- MEDLINE
DCOM- 20240229
LR  - 20240307
IS  - 1976-670X (Electronic)
IS  - 1976-6696 (Print)
IS  - 1976-6696 (Linking)
VI  - 57
IP  - 2
DP  - 2024 Feb
TI  - Glucosamine increases macrophage lipid accumulation by regulating the mammalian 
      target of rapamycin signaling pathway.
PG  - 92-97
AB  - 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 elementbinding 
      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. [BMB Reports 2024; 57(2): 92-97].
FAU - Kim, Sang-Min
AU  - Kim SM
AD  - Department of Biomedical Science, Program in Biomedical Science and Engineering, 
      Inha University, Incheon 22212, Korea.
FAU - Kim, Dong Yeol
AU  - Kim DY
AD  - Department of Biomedical Science, Program in Biomedical Science and Engineering, 
      Inha University, Incheon 22212, Korea.
FAU - Park, Jiwon
AU  - Park J
AD  - Department of Biomedical Science, Program in Biomedical Science and Engineering, 
      Inha University, Incheon 22212, Korea.
FAU - Moon, Young-Ah
AU  - Moon YA
AD  - Department of Molecular Medicine, College of Medicine, Inha University, Incheon 
      22212, Korea.
FAU - Han, Inn-Oc
AU  - Han IO
AD  - Department of Biomedical Science, Program in Biomedical Science and Engineering, 
      Inha University, Incheon 22212, Korea.
LA  - eng
PT  - Journal Article
PL  - Korea (South)
TA  - BMB Rep
JT  - BMB reports
JID - 101465334
RN  - N08U5BOQ1K (Glucosamine)
RN  - 0 (Lipopolysaccharides)
RN  - EC 2.7.1.1 (mTOR protein, mouse)
RN  - 0 (RNA, Messenger)
RN  - W36ZG6FT64 (Sirolimus)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - 0 (Transcription Factors)
SB  - IM
MH  - Animals
MH  - Mice
MH  - *Glucosamine/pharmacology
MH  - Lipopolysaccharides
MH  - Macrophages
MH  - RAW 264.7 Cells
MH  - RNA, Messenger
MH  - *Signal Transduction
MH  - Sirolimus
MH  - TOR Serine-Threonine Kinases
MH  - Transcription Factors
PMC - PMC10910086
COIS- CONFLICTS OF INTEREST The authors have no conflicting interests.
EDAT- 2023/11/15 06:42
MHDA- 2024/02/29 06:43
PMCR- 2024/01/04
CRDT- 2023/11/15 03:49
PHST- 2023/08/31 00:00 [received]
PHST- 2024/02/29 06:43 [medline]
PHST- 2023/11/15 06:42 [pubmed]
PHST- 2023/11/15 03:49 [entrez]
PHST- 2024/01/04 00:00 [pmc-release]
AID - 6039 [pii]
AID - bmb-57-2-92 [pii]
AID - 10.5483/BMBRep.2023-0158 [doi]
PST - ppublish
SO  - BMB Rep. 2024 Feb;57(2):92-97. doi: 10.5483/BMBRep.2023-0158.