Premium
Absence of toll‐like receptor‐2 (Tlr2) attenuates diet induced obesity and adipose tissue inflammation and insulin resistance
Author(s) -
Davis Jeremy E,
WalkerDaniels Jennifer,
Spurlock Michael E
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.907.9
Subject(s) - endocrinology , medicine , tlr2 , insulin resistance , adipose tissue , inflammation , insulin , tlr4 , chemistry , receptor , biology
Toll‐like receptor‐4 (Tlr4) is involved in fatty acid (FA) induced inflammation and insulin resistance. However, less is known about toll‐like receptor‐2 (Tlr2), which is also activated by FA. To investigate the involvement of this receptor in diet‐induced obesity (DIO) in mice, we utilized male Tlr2‐/‐ and 6J controls. Mice were fed either low fat (low‐fat control, LFC), high unsaturated fat (high‐fat control, HFC), or high saturated fat + palmitate (HFP) diets ad libitum for 16 weeks. Means were considered significant at P<0.05. These data showed that Tlr2‐/‐ mice were protected from DIO, but without significant changes in body weight, energy intake, or lipid profile. Serum monocyte chemotactic protein‐1 (MCP‐1) was lower in Tlr2‐/‐ mice fed the high fat diet. Transcript abundance of inflammation and oxidative stress markers in adipose tissue (AT), including tumor necrosis factor‐á, interleukin‐6, MCP‐1, F4/80, and nitric oxide synthase‐2 were attenuated in Tlr2‐/‐ mice. Furthermore, these effects were more pronounced in mice fed the HFP diet. Blood glucose and insulin were unchanged in Tlr2‐/‐ mice. However, stromal vascular cells isolated from AT of Tlr2‐/‐ mice had a marked increase in insulin sensitivity. These data indicate that Tlr2, as well as Tlr4, are involved in obesity‐induced inflammation and insulin resistance, specifically when fed a high saturated fat diet.