Objective   To explore whether the inflammatory stress can increase insulin resistance in the CD36 knockout (KO) mice.    Methods   After the mice were fed a standard chow for 14 weeks

oral glucose tolerance test

insulin release tests

lipids metabolism

SAA

IL-6

TNF-α and hepatic mRNA and proteins expression of mTOR

S6K

IRS-1

pIRS-1

2 were measured.    Results   Compared with the wide-type

the CD36 KO mice un-inflamed exhibited insulin resistance

and the insulin resistance index was increased[(3.01±1.24) vs (0.81±0.12)

P0.05]

the triglyceride level [(0.83±0.15) mmol/L vs (0.21±0.06) mmol/L，P0.05] together with the hepatic mRNA and protein expression of mTOR and S6K were increased while the IRS-1 expression were reduced

and the protein of pIRS-1

2 were raised. Compared with the CD36 KO un-inflamed control

the inflammatory group represented the elevated lever of insulin resistance[(4.65±1.54)vs(3.01±1.24)

P0.05]

triglyceride[(2.66±0.17) mmol/L vs(0.83±0.15)mmol/L

P0.05]

SAA[(13.62±5.05) ng/ml vs(5.74±1.54)ng/ml

P0.05]

IL-6[(43.81±1.23) pg/ml vs(35.24±4.13)pg/ml

P0.05]

TNF-α[(235.1±32.6) pg/ml vs(169.2±36.1)pg/ml

P0.05]

at the same time

the hepatic mRNA and proteins expression of mTOR and S6K were increased

while the hepatic mRNA and proteins expression of IRS-1 were reduced

also the protein of pIRS-1

2 were raised.    Conclusion   The inflammatory stress indeed increases insulin resistance in the CD36 knockout mice.