PMID- 24662749
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20140325
LR  - 20220330
IS  - 2044-4052 (Print)
IS  - 2044-4052 (Electronic)
IS  - 2044-4052 (Linking)
VI  - 4
IP  - 3
DP  - 2014 Mar 24
TI  - Effects of LPS and dietary free fatty acids on MCP-1 in 3T3-L1 adipocytes and 
      macrophages in vitro.
PG  - e113
LID - 10.1038/nutd.2014.10 [doi]
AB  - BACKGROUND: High levels of free fatty acids (FFA) have been suggested to be one 
      of the underlying mechanisms for adipose tissue (AT) inflammation and dysfunction 
      in obesity. Human AT produces several adipokines including monocyte 
      chemoattractant protein-1 (MCP-1), which are involved in the pathogenesis of 
      obesity-mediated inflammation. OBJECTIVE: In this study, we investigated the 
      effects of lipopolysaccharide (LPS) and a panel of dietary FFA on MCP-1 gene and 
      protein expression in adipocytes and macrophages. Furthermore, we investigated 
      whether the effect of LPS and FFA were mediated through the toll-like receptor 4 
      (TLR4). METHODS: 3T3-L1 adipocytes and THP-1 macrophages were incubated for 24 h 
      with the following FFA: monounsaturated fatty acid (oleic acid), saturated fatty 
      acid (palmitic acid) and trans fatty acid (elaidic acid; 500 muM) with and without 
      LPS (2 ng ml(-1)), and MCP-1 and TLR4 mRNA expression and MCP-1 protein secretion 
      was determined. RESULTS: The results showed that LPS significantly increased 
      MCP-1 and TLR4 expression and MCP-1 secretion in 3T3-L1 adipocytes, and that the 
      MCP-1 expression was blocked by a TLR4 inhibitor (CLI095). The effects of the 
      various FFA on MCP-1 mRNA expression and protein secretion in the adipocytes 
      showed no significant changes either alone or in combination with LPS. In 
      macrophages, palmitic acid increased MCP-1 mRNA expression by 1.8-fold (P<0.05), 
      but oleic acid and elaidic acid had no effects. CONCLUSIONS: In conclusion, in 
      3T3-L1 adipocyte, the TLR4-agonist, LPS, stimulates the proinflammatory chemokine 
      MCP-1. The different classes of FFA did not induce MCP-1 mRNA expression or 
      protein secretion in the adipocytes, but the saturated FFA, palmitic acid, 
      induced MCP-1 mRNA expression in macrophages, possibly because of the higher 
      expression level of TLR4 in the macrophages than the adipocytes. Our results 
      indicate that FFA may induce AT inflammation through proinflammatory stimulation 
      of macrophages.
FAU - Cullberg, K B
AU  - Cullberg KB
AD  - Department of Endocrinology and Internal Medicine, MEA, THG, Aarhus University 
      Hospital, Aarhus C, Denmark.
FAU - Larsen, J O
AU  - Larsen JO
AD  - Department of Endocrinology and Internal Medicine, MEA, THG, Aarhus University 
      Hospital, Aarhus C, Denmark.
FAU - Pedersen, S B
AU  - Pedersen SB
AD  - Department of Endocrinology and Internal Medicine, MEA, THG, Aarhus University 
      Hospital, Aarhus C, Denmark.
FAU - Richelsen, B
AU  - Richelsen B
AD  - Department of Endocrinology and Internal Medicine, MEA, THG, Aarhus University 
      Hospital, Aarhus C, Denmark.
LA  - eng
PT  - Journal Article
DEP - 20140324
PL  - England
TA  - Nutr Diabetes
JT  - Nutrition & diabetes
JID - 101566341
PMC - PMC3974034
EDAT- 2014/03/26 06:00
MHDA- 2014/03/26 06:01
PMCR- 2014/03/01
CRDT- 2014/03/26 06:00
PHST- 2013/09/10 00:00 [received]
PHST- 2014/01/23 00:00 [revised]
PHST- 2014/02/07 00:00 [accepted]
PHST- 2014/03/26 06:00 [entrez]
PHST- 2014/03/26 06:00 [pubmed]
PHST- 2014/03/26 06:01 [medline]
PHST- 2014/03/01 00:00 [pmc-release]
AID - nutd201410 [pii]
AID - 10.1038/nutd.2014.10 [doi]
PST - epublish
SO  - Nutr Diabetes. 2014 Mar 24;4(3):e113. doi: 10.1038/nutd.2014.10.