High fat intake induces a population of adipocytes to co-express TLR2 and TNFalpha in mice with insulin resistance.
Cytokine production in fat tissue plays a key role in insulin resistance. The aim of study is to know the phenotypic changes of adipocytes with high fat-induced insulin resistance. High fat intake induced the expression of tumor necrosis factor alpha (TNFalpha) in visceral fat tissue as well as development of insulin resistance. Analysis of the gene expression profiles in adipocytes showed that high fat intake induced the expression of toll-like receptor 2 (TLR2) in addition to TNFalpha. Flow cytometry analysis revealed the presence of adipocytes co-expressing TLR2 and TNFalpha (TLR2/TNFalpha-adipocytes), and the number of TLR2/TNFalpha-adipocytes in visceral fat tissues was increased by high fat intake compared to that in subcutaneous fat tissues. Free fatty acids increased TNFalpha expression in 3T3-L1 adipocytes through TLR2 signals. These results indicate that TLR2/TNFalpha-adipocytes possibly cause the induction of TNFalpha expression in visceral fat tissues, being associated with the development of high fat-induced insulin resistance.
Murakami
Kentaro
K
Department of Clinical Cell Biology, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.
Bujo
Hideaki
H
Unoki
Hiroyuki
H
Saito
Yasushi
Y
D041721:3T3-L1 Cells; D017667:Adipocytes / Q000378:metabolism*; D000818:Animals; D005223:Fats / Q000008:administration & dosage / Q000378:metabolism*; D005434:Flow Cytometry; D005786:Gene Expression Regulation; D007333:Insulin Resistance / Q000235:genetics / Q000502:physiology*; D051379:Mice; D010641:Phenotype; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051195:Toll-Like Receptor 2 / Q000235:genetics / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism*
D005223:Fats; D012333:RNA, Messenger; D051195:Toll-Like Receptor 2; D014409:Tumor Necrosis Factor-alpha