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Please use this identifier to cite or link to this item: http://142.54.178.187:9060/xmlui/handle/123456789/12960
Title: Chlorogenic acid inhibits forming of diabetes mellitus in rats induced by high-fat high-sucrose and streptozotocin
Authors: Wang, Yan
Peng, Shuguang
Mei, Zihan
Jin, Chenzhong
Kang, Jinhe
Xiang, Minghui
Wang, Zheng
Hu, Yihong
Keywords: Chlorogenic acid
Type 2 diabetes mellitus
high-fat high-sucrose diet
hepatic glucose-6-phosphatase
skeletal muscle glucose transporter 4
Issue Date: 14-May-2020
Publisher: Karachi:Pakistan Journal of Pharmaceutical Sciences, university of Karachi.
Citation: Wang, Y., Peng, S., Mei, Z., Jin, C., Kang, J., Xiang, M., ... & Hu, Y. (2020). Chlorogenic acid inhibits forming of diabetes mellitus in rats induced by high-fat high-sucrose and streptozotocin. Pakistan Journal of Pharmaceutical Sciences, 33(3).
Abstract: To evaluate the inhibitory effect of chlorogenic acid on the forming of type 2 diabetes mellitus (T2DM), using Sprague Dawley (SD) rats, a recognized T2DM model induced by high-fat high-sucrose diet (HFSD) and streptozotocin (STZ). Thirty female SD rats were assigned equally to three groups randomly: normal control with standard commercial (NC), chlorogenic acid treatment with HFSD and chlorogenic acid (90mg/kg, CA), and diabetes model with HFSD (DM). Upon treatment with chlorogenic acid, suppression of the onset of diabetes, reduced serum glucose and insulin concentrations, improved glucose tolerance and increased body weight and visceral fat weight were observed. Serum triglyceride, total cholesterol, low density lipoprotein levels, and kidney and pancreas morphology were significantly ameliorated. Chlorogenic acid also inhibited the mRNA levels of hepatic G-6-Pase and up-regulated the mRNA levels of skeletal muscle GLUT4. Our results indicated that before the onset of diabetes, chlorogenic acid had an inhibitory effect against the forming of T2DM induced by HFSD and STZ through regulating the glucose and lipid metabolism.
URI: http://142.54.178.187:9060/xmlui/handle/123456789/12960
ISSN: 1011-601X
Appears in Collections:Issue 3

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