关键词: 胰岛素抵抗, 胰高血糖素样肽-1, 白介素-6, N-乙酰半胱氨酸

Abstract: Objective  To investigate the effects of N-acetylcysteine (NAC) on serous glucagon likepeptide-1(GLP-1) and interleukin-6(IL-6) expressions in the hepatic and pancreas tissues of SD rats which were insulin resistant after high-fat forage. Methods  A total of 40 healthy adult male SD rats were randomly divided into two groups: control group (NC group, n=10), fed with normal diet; high-fat group (HF group, n=30), fed with fat-rich diet to construct models of insulin resistance. After 12 weeks, fasting plasma glucose (FPG), fasting insulin (FIns), serum lipids, insulin sensitivity and insulin resistance index (HOMA-IR) were detected to confirm the construction of models. The HF group was randomly subdivided into high fat control group (HFN group, n=15), and high fat+NAC group (HF+NAC group, n=15). Rats in the HF+NAC group were given NAC 300mg/(kg·d)by gavage once a day with high-fat diet simultaneously. Rats in NC group and HFN group were given the same volume of physiological saline with the same method. After 4 weeks, blood samples were collected from angula vein to test FPG, FIns and blood lipid levels. Meanwhile, the pathological changes of liver were observed under light microscope after HE staining. The serum level of GLP-1 was examined by enzyme-linked immunoassay (ELISA). The expression of IL-6 in the hepatic tissues and pancreas was detected by immunohis-tochemistry. Results  In HFN group, the sensitivity to insulin decreased,glucose tolerance impaired, and fatty liver occurred. Serous level of GLP-1 significantly increased in HF+NAC group compared with HFN group (P<0.05); the expression of IL-6 in the liver and pancreas tissues in HF+NAC group was much lower than that of the control group (P<0.05). Conclusion  NAC would reduce the insulin resistance in high-fat-diet rats by increasing the serous level of GLP-1 while reducing IL-6 protein expression and activity, which has a protective effect on insulin resistance.

Key words:  N-acetylcysteine, Glucagon likepeptide-1, Insulin resistance, Interleukin-6