• Title/Summary/Keyword: hyperlipidemic dietary mice

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Regulatory Effects of Cheunggansoyo-san on Pathophysiological Changes Induced by Hyperlipidemic Diets in the Mice

  • Park Kyung-Ho;NamGung Uk;Lee Yong-Koo;Kang Tak-Lim;Kim Dong-Hee
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.19 no.6
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    • pp.1629-1635
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    • 2005
  • Hyperlipidemia is caused by high dietary intake of cholesterol and saturated fats, and is known as a major risk factor for atherosclerosis. In the oriental medicine, Cheunggansoyo-san (CGSYS) has been used for supplementing hematopoietic function and for treating cardiovascular disorders. In the present study, CGSYS was administered into hyperlipidemic mice. Increases in body weight and cholesterol levels induced by hyperlipidemic diets for 6 weeks were significantly inhibited by CGSYS administration. Serum levels of glucose, triglyceride, SGOT, and SGPT values were all decreased by CGSYS treatment compared with hyperlipidemic dietary mice. Moreover, CGSYS decreased LDL-cholesterol, but increased HDL-cholesterol levels in hyperlipidemic mice. Thus, the present results suggest that CGSYS appears to De effective for down-regulating risk factors of hyperlipidemia.

The Effect of Jeseubsungi-tang on Dietary Hyperlipidemia-induced Mice (제습순기탕(除濕順氣湯)이 고지혈증(高脂血症) 병태(病態) 모델에 미치는 영향(影響))

  • Kim, Jung-Hyun;Jo, Hyun-Kyung;Yoo, Ho-Rhyong;Seol, In-Chan;Kim, Yoon-Sik
    • The Journal of Internal Korean Medicine
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    • v.27 no.1
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    • pp.16-26
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    • 2006
  • Objectives : This experiment was performed to determine the effects of the Jeseubsungi-tang(JSSGT) on hyperlipidemia-induced by hypercholesterolemic diet in mice. Methods : C57BL/6 mice were sensitized with a hypercholesterolemic diet for 6 weeks. Experimental group was treated with $150mg/d{\ell}$ concentrations of JSSGT for 4 weeks (once a day). Results: JSSGT-treated mice showed a body weight decrease compared to normal group. JSSGT-treated mice showed a significant decrease in cholesterol, total cholesterol, triglyceride, ALT and LDL-cholesterol levels compared to hyperlipidemia-induced control group. However, HDL-cholesterol levels in JSSGT-treated group significantly increased compared to the hyperlipidemia-induced control group. Conclusion : These results suggest that JSSGT is effective in treating hyperlipidemia. Because only hyperlipidemic mice were studied, further research is needed.

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Effect of conjugated linoleic acid in diacylglycerol-rich oil on the lipid metabolism of C57BL/6J mice fed a high-fat high-cholesterol diet

  • Lee, Jeung Hee;Cho, Kyung-Hyun;Lee, Ki-Teak
    • Korean Journal of Agricultural Science
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    • v.41 no.1
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    • pp.47-58
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    • 2014
  • The effect of conjugated linoleic acid (CLA) isomers esterified in diacylglycerol (DAG)-rich oil on lipid metabolism was investigated. Since dietary DAG has been known to induce the regression of atherosclerosis, CLA-DAG and olive-DAG oils containing similar levels of DAG (51.4~54.2%) were synthesized from olive oil. Hyperlipidemic C57BL/6J mice were then fed high-fat high-cholesterol diets supplemented with these oils (5% each) for 7 wk. The CLA-DAG diet containing 2.1% CLA isomers (0.78% c9,t11-CLA; 1.18% t10,c12-CLA) remarkably increased the levels of total plasma cholesterol and glutamic oxaloacetic transaminase (GOT) along with hepatic cholesterol and triacylglycerol (TAG) contents. Furthermore, the CLA-DAG diet inhibited fat uptake into adipose tissue whereas fat deposition (especially in the liver) was increased, resulting in the development of fatty livers. Hepatic fatty acid composition in the CLA-DAG mice was different from that of the olive-DAG mice, showing higher ratios of C16:1/C16:0 and C18:1/C18:0 in the liver. The activity of hepatic acyl-CoA:cholesterol acyltransferase (ACAT) was higher in CLA-DAG mice while plasma lecithin:cholesterol acyltransferase (LCAT) activity and the ferric reducing ability of plasma (FRAP) were lower in CLA-DAG mice compared to the olive-DAG animals. Results of the present study suggest that CLA incorporation into DAG oil could induce atherosclerosis in mice.