Effects of Sangtong alkaloids on blood glucose and hepatic insulin resistance in db/db mice with type 2 diabetes mellitus
10.3969/j.issn.1001-1528.2017.05.001
- VernacularTitle:桑酮碱对2型糖尿病db/db小鼠血糖及肝脏胰岛素抵抗的影响
- Author:
Xin SUN
;
Zhi MA
;
Qinghai MENG
;
Meiyu KUAI
;
Ying LU
;
Yi JING
;
Chao LIN
;
Yu LI
;
Huimin BIAN
- Keywords:
Sangtong alkaloids;
type 2 diabetes;
liver;
insulin resistance;
total flavonoids from mulberry leaves;
total alkaloids from mulberry leaves
- From:
Chinese Traditional Patent Medicine
2017;39(5):885-890
- CountryChina
- Language:Chinese
-
Abstract:
AIM To explore the effects of Sangtong alkaloids (total alkaloids and total flavones from Mori folium,STA) on the random blood glucose,starch tolerance and hepatic insulin resistance in db/db mice with type 2 diabetes mellitus.METHODS Eight-week-old db/db mice were divided into model group (normal saline),acarbose group (39 mg/kg) and Sangtong alkaloids groups (105,210 and 420 mg/kg),db/m mice were used as control group (normal saline).The mice were given by intragastric administration for one hundred days.The random blood glucose of mice was determined every ten days.The starch tolerance was determined in the 100th day,together with the determination of serum insulin level,insulin resistance index and insulin sensitivity index.Histopathology changes of pancreas were observed by HE staining.Protein expressions of P-IRS1,P-PI3 K,P-AKT and GLUT2 were detected by Western blot.RESULTS Sangtong alkaloids significantly decreased the random blood glucose,serum insulin level and insulin resistance index,and increased the insulin sensitivity index in db/db mice.Meanwhile,Sangtong alkaloids ameliorated the pancreas histopathological damage and up-regulated the protein expressions of P-IRS1,P-PI3K,P-AKT and GLUT2 in liver.CONCLUSION Sangtong alkaloids can decrease the random blood glucose and improve the insulin resistance of liver in db/db mice with type 2 diabetes mellitus,whose mechanism may be associated with the regulation of hepatic insulin signal pathway.