Inflammatory Stress Induce Insulin Resistance In The Liver In The CD36 Knockout Mice

Objective To explore whether the inflammatory stress can increase insulin resistance in the CD36 knockout 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-αand 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±1.24vs0.81±0.12,P<0.05), the triglyceride level (0.83±0.15vs0.21±0.06 mmol/l,P<0.05) 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±1.54vs3.01±1.24,P<0.05),triglyceride(2.66±0.17vs0.83±0.15mmol/l,P<0.05),SAA(13.62±5.05vs5.74±1.54ng/ml,P<0.05),IL-6(43.81±1.23vs35.24±4.13pg/ml,P<0.05),TNF-α(235.1±32.6vs169.2±36.1pg/ml,P <0.05), 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.Conclusions The inflammatory stress indeed increase insulin resistance in the CD36 knockout mice.