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Toll‐like receptor‐4 (TLR‐4) deficiency did not offer protection against trans fat or high fat diet‐induced hyperinsulinemia and hyperglycemia in mice
Author(s) -
Ganji Vijay,
VijayKumar Matam,
Aitken Jesse,
Gewirtz Andrew T
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.221.2
Subject(s) - medicine , endocrinology , hyperinsulinemia , insulin resistance , inflammation , adiponectin , type 2 diabetes , insulin , hyperinsulinism , leptin , obesity , diabetes mellitus
Low‐grade chronic inflammation is linked to insulin resistance, type‐2 diabetes, obesity, and atherosclerosis. TLR‐4 signaling plays an important role in inflammation. It has been reported that TLR‐4 deficiency offers protection against obesity and inflammatory response induced by diets high in fat. We investigated whether natural TLR‐4 mutation (BL‐10 background) protects against trans fat (TF) and high fat (HF) induced insulin resistance, hyperglycemia, and hyperleptinemia. TLR‐4 deficient and wild‐type (WT) mice were fed either low fat control (LF; 4.5%), TF (35%), or HF (35%) diets ad libitum for 12 weeks. Both groups of mice had significantly higher serum insulin, glucose, cholesterol, and leptin in response to TF and HF diets compared to LF control (P<0.05). Mice fed TF diet had hepatomegaly regardless of TLR‐4 genotype. There was no significant difference in serum insulin, glucose, and triacylglycerol between TLR‐4 deficient and WT mice fed LF, TF, or HF diets. There was a tendency toward higher serum cholesterol in TLR‐4 deficient mice compared to WT mice, in all three diet groups. Neither TLR‐4 genotype nor diet type had effect on serum adiponectin. These data suggest that lack of TLR‐4 signaling does not confer protection against TF or HF induced hyperinsulinemia and hyperglycemia in BL‐10 mice. Supported by Intramural Grant from the College of Health and Human Sciences, Georgia State University.