To investigate the effects of chronic intermittent hypoxia on the expression of PTP-1B and IRS-1 and the possible mechanism of insulin resistance caused by chronic intermittent hypoxia.

According to the principle of random number,twenty-four healthy male SD rats were divided into the normal group(NC group),the four-week chronically intermittent hypoxia group(CIH4 group)and the eight-week chronically intermittent hypoxia group(CIH8 group) equally. The NC group were raised normally, while the CIH4 and the CIH8 ones were exposed to the intermittent hypoxia cabins from 9 am to 5 pm,in which the lowest air concentration was 6%- 7%.The fast blood glucose(FBG) and fasting insulin(FINS) were detected at the fourth week and the eighth week to evaluate the insulin insistence with homeostasis model assessment-insulin resistance index(HMOA-IR)and insulin sensitive index(ISI),and the average gray value indicating the expression of PTP-1B and IRS-1 protein was tested with SABC immunohistochemical kits,of which the data were analysed statistically.

Compared to the NC group,FBG,insulin level and HOMA-IR of the CIH4,CIH8 group increased while ISI decreased (P< 0.05),and the trend is more obvious in CIH8 group.Compared to the NC group,PTP-1B protein rised and IRS-1 protein declined in the expression of the CIH4 and CIH8 group(P< 0.05).Pearson correlation analysis showed that HOMA-IR was negatively correlated with the gray value of PTP-1B and positively corrected with that of IRS-1,ISI had a positive relationship with PTP-1IR and a negative relationship with that of IRS-1.

①The exposure of chronically intermittent hypoxia caused increased FNG,insulin level and insulin resistence,which exacerbated as the exposure time extended.②The chronically intermittent hypoxia induced high expression of PTP-1B protein and low expression of IRS-1 in rats'liver cells. PTP-1B and IRS might participate in the insulin resistence of rats caused by chronically intermittent hypoxia.

Chronic intermittent hypoxia; Protein tyrosine phosphatase-1B; Insulin receptor substrate-1; Insulin resistance