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Hillgartner, F.B., Salati, L.M. and Goodridge, A.G, “Physiological and molecular mechanisms involved in nutritional regulation of fatty acid synthesis,” Physiol Rev, 75. 47-76. 1995.

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Article

Effects of High Hydrostatic Pressure Extract of Korean Fresh Ginseng on Hepatic Lipid Accumulation and AMPK Activation in HepG2 Cells

1Department of Nutritional Science and Food Management, Ewha Womans University, Seoul, Republic of Korea

2Research Group of Convergence Technology, Korea Food Research Institute, Seongnam, Gyeonggi, Republic of Korea

3Department of Food and Nutrition, Korea University, Seoul, Republic of Korea


Journal of Food and Nutrition Research. 2015, Vol. 3 No. 1, 40-45
DOI: 10.12691/jfnr-3-1-7
Copyright © 2015 Science and Education Publishing

Cite this paper:
Mak-Soon Lee, Yoonjin Shin, Sunyoon Jung, Chong-Tai Kim, In-Hwan Kim, Yangha Kim. Effects of High Hydrostatic Pressure Extract of Korean Fresh Ginseng on Hepatic Lipid Accumulation and AMPK Activation in HepG2 Cells. Journal of Food and Nutrition Research. 2015; 3(1):40-45. doi: 10.12691/jfnr-3-1-7.

Correspondence to: Yangha  Kim, Department of Nutritional Science and Food Management, Ewha Womans University, Seoul, Republic of Korea. Email: yhmoon@ewha.ac.kr

Abstract

Ginseng is widely used as a medicinal herb and has demonstrated effects against liver diseases. The aim of this study is to investigate the hypolipidemic effects of the high hydrostatic pressure extract of Korean fresh ginseng (HEG) on hepatic lipid accumulation in HepG2 cells. The intracellular triglyceride and cholesterol contents were determined using enzymatic colorimetric methods. The mRNA levels of fatty acid synthase (FAS) and 3-hydroxy-3-methyl-glutaryl CoA reductase (HMGCR) were assayed by quantitative real-time PCR. The activity of AMP-activated protein kinase (AMPK) was measured with an AMPK kinase assay kit. HEG significantly reduced hepatic triglyceride and cholesterol contents in HepG2 cells. Furthermore, HEG suppressed the expression of FAS, a key enzyme in fatty acid synthesis, and HMGCR, a rate-limiting enzyme in hepatic cholesterol synthesis. Additionally, HEG increased the activity of AMPK, a major regulator of lipid metabolism. These results suggest that HEG reduces hepatic lipid accumulation with inhibition of FAS and HMGCR expression and stimulation of AMPK activity in HepG2 cells. Consequently, HEG may be beneficial as a functional food ingredient to improve various hepatic diseases by reducing hepatic lipid accumulation.

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