The Effect Of Trimethyl-apigenin In Metabolic Syndrome Mice Due To Intervention Of Monosodium Glutamate And Overnutrition During Lactation

Objective: The aim of this study was to establish a full metabolic syndrome mice model through intervention of monosodium glutamate (newborn) and overnutrition during lactation. Methods: Select normal number of newborn male mice, then randomly divided into two groups. MSG was subcutaneously injected (3mg/g/day, 10ul/g/day) to the overnutition group, which was achieved by litter-enshorten to 5 pups per mother from day 2 after birth until weaning (MSG combine overnutrition group). While the same volume of physiological solution (10ul/g/day) was injected to the balenced nutrition group, which was 10 pups per mother from day 2 after birth until weaning, for 7 consecutive days(d2-d8). After weaning (21 d), the mice were feeding daptivly until 16-week-old, meared body weight, body length and waist circumference of each mouse wihtout anaesthesia. Serum levels of glucose, triglyceride, total cholesterol, insulin of each group were measured. After been sacrificed, organs and adipose tissues of each mouse were weighted, frozen and prepared for testing. Results:①Compared with Control, the body weight, waist circumference, LEE index, subcutaneous fat and visceral fat weight of 16-week-old mice have significantly increased in Vehicle(p<0.05).②Blood glucose, triglyceride, total cholesterol, insulin of monosodium glutamate combine overnutrition treated mice showed various degree of increase, insulin resistance also has been emerged. Conclusion: In the present study, intervention of monosodium glutamate and overnutrition during lactation can cause significant obesity in mice, leading to a comprehensive model of metabolic syndrome, including: central obesity, hyperglycaemia, hyperlipidemia, hypercholesterolemia, hyperinsulinemia and insulin resistance. Objective: To investigate the machanism of TMA on anti-metabolic syndrome in a MetS mice model, which was induced by intervention of monosodium glutamate (newborn) and overnutrition during lactation. Methods: Monosodium glutamate combine overnutrition-trated or saline-treated newborn male mice were weaned. After been feeding adaptivly for one week, they were randomly divided into 6 different groups(n=10 or 9 mice per group) at 4 weeks of age:①saline-treated + balenced nutrition + vehicle (Control, n=10);②monosodium glutamate-treated + overnutrition + vehicle (Vehicel, n=10);③④⑤monosodium glutamate-treated + overnutrition + Trimethyl-apigenin 5/10/20mg/kg group (TMA 5, n=9; TMA 10, n=10; TMA 20, n=20);⑥monosodium glutamate-treated + overnutrition + rosiglitazone 5mg/kg group (RGZ 5, n=9). Control group and Vehicel group were administered equipotent volume of vehicle. TMA 5/10/20 group were administered Trimethyl-apigenin with at a dose of 5/10/20 mg/kg body weight per day. RGZ 5 group were administered rosiglitazone with at a dose of 5 mg/kg body weight per day. The mice were feeding daptivly until 16-week-old, meared body weight, body length, waist circumference wihtout anaesthesia. Serum levels of glucose, triglyceride, total cholesterol, insulin of each group were measured. After been sacrificed organs and adipose tissue of each mouse were weighted, frozen, prepared for testing. RT-PCR detection the mRNA expression levels of peroxisome proliferator-activated receptors (PPARα, PPARβ/δ, PPARγ) and adiponectin in mice's liver. Result:①In the present study, TMA has played a significant role in weight loss in MSG combine overnutrition mice, comparing with the Vehicle group. 5mg/kg/day rosiglitazone showed no effect on body weight lose.②TMA 10mg/kg/day can improve glucose and lipid metabolism in this mice model, especially shows a significant hypoglycemic and decreased the total cholesterol effect, furthermore, it also can significantly improve insulin resistance, and the effct tensity is considerable to rosiglitazone 5mg/kg/d.③We detected genes expression in the hapatic tissues of each group. Compared with the Vehicle group, TMA enhanced the mRNA expression of PPARα, PPARβ/δand Adiponectin, while no significant effect on the mRNA expression of PPARγin hapatic of metabolic syndrome mice model through intervention of monosodium glutamate (newborn) and overnutrition during lactation. Conclusion:The result suggested that Trimethyl-apigenin has a comprehensive role in the anti-metabolic syndrome, the effects are as follows: weight loss, improving glucose and lipid metabolism, improving insulin resistance. Mean while, TMA enhanced the mRNA expression of PPARα, PPARβ/δand Adiponectin, while no significant effect on the mRNA expression of PPARγin hapatic. Therefore, Trimethyl-apigenin is likely to be a useful clinical drug to prevent and treat metabolic syndrome in the future.