Compound K attenuates glucose intolerance and hepatic steatosis through AMPK-dependent pathways in type 2 diabetic OLETF rats
| Autor: | Da-Hee Oh, Sang Yeoul Lee, Kyu-Jeong Ahn, Sung Hyun Chung, Ho-Yeon Chung, Moon Chan Choi, In-Kyung Jeong, Yoo-Cheol Hwang, Sung-Jig Lim |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Blood Glucose Male medicine.medical_specialty Ginsenosides Seoul Rats Inbred OLETF 03 medical and health sciences 0302 clinical medicine Insulin resistance AMP-activated protein kinase Japan Internal medicine Glucose Intolerance Republic of Korea medicine Animals Carnitine Endocrinology-Metabolism biology business.industry AMP-activated protein kinases Fatty liver Ginsenoside M1 AMPK Diabetes mellitus type 2 medicine.disease Metformin Rats Fatty acid synthase 030104 developmental biology Endocrinology Liver 030220 oncology & carcinogenesis biology.protein Original Article Steatosis business Protein Kinases medicine.drug Non-alcoholic fatty liver disease |
| Zdroj: | The Korean Journal of Internal Medicine |
| ISSN: | 2005-6648 1226-3303 |
| Popis: | Background/aims Non-alcoholic fatty liver disease is associated with insulin resistance. Compound K (CK) is the final metabolite of panaxadiol ginsenosides that have been shown to exert antidiabetic effects. However, the molecular mechanism of the antidiabetic effects in the liver have not been elucidated; further, whether CK has beneficial effects in hepatosteatosis remains unclear. Therefore, we evaluated the effect of CK on hepatosteatosis as well as its mechanism in high-fat diet (HFD)-fed type 2 diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats. Methods Twenty-four-week-old male OLETF rats were assigned to four groups: control (saline), CK 10 mg/kg, CK 25 mg/kg, or metformin 300 mg/kg (positive control); all treatments were administered orally for 12 weeks. Results Fasting glucose levels of the CK25 group were significantly lower than those of the control group during the 12 weeks. The results of the oral glucose tolerance test showed that both the glucose concentration after glucose loading and the fasting insulin levels of the CK25 group were significantly lower than those of the control. Hepatosteatosis was significantly improved by CK25. CK25 and metformin significantly increased the phosphorylation of hepatic adenosine monophosphate-activated protein kinase (AMPK). CK25 significantly inhibited the expression of sterol regulatory element-binding protein-1c and fatty acid synthase, while upregulating that of peroxisome proliferator-activated receptor-α and carnitine palmitoyltransferase-1. Conclusions CK improved glucose intolerance and hepatosteatosis in HFD-fed OLETF rats through AMPK activation, which has dual mode of action that involves decreasing the synthesis of fatty acids and increasing fatty acid oxidation. |
| Databáze: | OpenAIRE |
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