动物造模,2型糖尿病 z-bio 2022-07-21 472

　　Objective: To study the effect of camel milk (CM) on body weight, blood glucose, blood lipid, insulin, PPARγ and TNF-α gene expression in type 2 diabetic rats.

　　Methods: Rat models of type 2 diabetes were induced by intraperitoneal injection of high-fat diet and low-dose (30 mg/kg) streptozotocin (STZ). model) group, camel milk low dose (CM-L) group (3.5 mg/kg d), camel milk high dose (CM-H) group (10 mg/kg d), body weight and blood sugar were measured weekly, and the first Glucose tolerance test was performed for 4 weeks, and the rats were sacrificed by decapitation after 4 weeks of administration. The levels of blood lipids (TC, TG, HDL-C, LDL-C) and insulin were measured, and the mRNA expressions of PPARγ in adipose tissue and TNF-α in liver tissue were detected.

　　Results: Compared with the normal control group, the body weight of the rats in the model group decreased significantly (P < 0.01), and the fasting blood glucose, glucose tolerance 0, 30, 60, and 120 min blood glucose, and serum TC, TG and LDL-C levels were significantly increased. (P < 0.01), HDL-C content decreased and insulin level increased. CM could alleviate the weight loss of diabetic rats and reduce hyperglycemia. The CM-H group achieved a significant hypoglycemic effect at the 4th week of administration, and significantly reduced glucose tolerance for 30 minutes (P < 0.05). CM has a tendency to reduce TC, TG, LDL-C content, increase HDL-C content, and decrease insulin in diabetic rats, and CM-H dose group can significantly reduce TG and LDL-C content (P < 0.05). Compared with the normal control group, the PPARγ mRNA in the model group was significantly down-regulated (P < 0.05), and the TNF-α mRNA was significantly up-regulated (P < 0.01). P < 0.05), CM can reduce its TNF-α mRNA expression.

　　Conclusion: CM can alleviate the weight loss of type 2 diabetic rats, improve the symptoms of hyperglycemia, impaired glucose tolerance, dyslipidemia, etc. The mechanism may be related to the regulation of PPARγ and TNF-α expression.