Objective: To study the effect of camel milk (CM) on the body weight, blood glucose, blood lipid, insulin, PPARγ and TNF-α gene expression in type 2 diabetic rats.
Method: In the normal control group, the model group (model) is divided into high-fat diet and intraperitoneal injection of a small amount of streptozotocin (STZ) to induce type 2 diabetes in rats. 4 groups. The body weight and blood glucose levels of the camel milk low-dose (CM-L) group (3.5 mg/kg d) and camel milk high-dose (CM-H) group (10 mg/kg d) were measured once a week. The glucose tolerance test was performed for 4 weeks. Four weeks after administration, the animals were killed by hair loss, blood lipids (TC, TG, HDL-C, LDL-C) and insulin levels were measured, and the expression of PPARγ in adipose tissue was measured. Detect TNF-αmRNA in liver tissue.
Results: Compared with the normal control group, the weight of the rats in the model group was significantly reduced (P \u003cu\→ u0.01c0.01), fasting blood glucose, glucose tolerance were 0, 30, 60, 120 minutes, and serum TC and TG , LDL-C content increased significantly (P \u003cu003c0.01), HDL-C content decreased, and insulin level increased. CM can reduce weight loss and hyperglycemia in diabetic rats. The CM-H group achieved a significant hypoglycemic effect after 4 weeks of administration, and significantly reduced glucose tolerance to 30 minutes blood glucose level (P\u003c0.05). CM tends to reduce the content of TC, TG, LDL-C in diabetic rats, increase the content of HDL-C and reduce insulin. The CM-H group can significantly reduce the content of TG and LDL-C (P\u003c0.05). Compared with the normal control group, PPARγmRNA in the model group was significantly down-regulated (P\u003c0.05), while TNF-αmRNA was significantly up-regulated (P\u003c0.01). CM increases PPARγmRNA in diabetic rats. The difference in the CM-H group was statistically significant (P\u003c0.05). ), CM can reduce its TNF-αmRNA expression.
Conclusion: CM can reduce weight loss in type 2 diabetic rats and improve symptoms such as hyperglycemia, impaired glucose tolerance and dyslipidemia. This mechanism may be related to the regulation of PPARγ and TNF-α expression.