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Article

Supplementation of Non-Fermented and Fermented Red Ginseng Improves Obese Phenotypes, Lipid and Inflammatory Profiles, and Antioxidant Defense System in High Fat-Fed Rats

1Research Center for Food and Bio Convergence, Department of Food Science, Sun Moon University, Asan, Chungchengnam-do, 31460, Republic of Korea

2Institute of Sports Health Science, Sun Moon University, Asan, Chungchengnam-do, 31460, Republic of Korea


Journal of Food and Nutrition Research. 2021, Vol. 9 No. 3, 154-162
DOI: 10.12691/jfnr-9-3-8
Copyright © 2021 Science and Education Publishing

Cite this paper:
Soyeon Jeong, Misun Park, Minji Kang, Yeong-Ju Park, Minkyeong Lee, Cheongbin You, Unsik Hwang, Youngju Song, Hoon Park, Sunhye Lee, Heejae Suh. Supplementation of Non-Fermented and Fermented Red Ginseng Improves Obese Phenotypes, Lipid and Inflammatory Profiles, and Antioxidant Defense System in High Fat-Fed Rats. Journal of Food and Nutrition Research. 2021; 9(3):154-162. doi: 10.12691/jfnr-9-3-8.

Correspondence to: Heejae  Suh, Research Center for Food and Bio Convergence, Department of Food Science, Sun Moon University, Asan, Chungchengnam-do, 31460, Republic of Korea. Email: lsh71300@sunmoon.ac.kr; suhhj@sunmoon.ac.kr

Abstract

Obesity is characterized by excessive fat accumulation, chronic inflammation, and enhanced oxidative stress that can present a substantial risk for metabolic complications. The aim of this study was to investigate the protective effects of red ginseng (RG), and its bio-transformed form (fermented RG, FRG) by microorganism on obese phenotype, lipid profile, and inflammation and oxidant profiles in rats fed a high-fat (HF) diet. FRG was prepared by fermentation of RG with Lactobacillus pentosus KCCM 12762P. Male Sprague-Dawley rats (n = 8/group; 6 weeks old) were counterbalanced by initial weight into four groups and fed either a low-fat (LF; 10% kcal as fat), high-fat (HF; 45% kcal as fat), or HF diet supplemented with RG or FRG at 1% (w/w) in diet for 6 weeks. General phenotypes (body weight, energy intake, visceral adiposity), lipid and inflammatory profiles, and oxidative states were assessed. RG and FRG supplementation suppressed HF-induced upregulation of proinflammatory cytokine genes, interleukin-6 and tumor necrosis factor alpha, in both white adipose and liver tissues. Similarly, RG and FRG partially reversed HF-induced downregulation of antioxidant enzymes at the gene level. Concomitantly, RG and FRG reduced body weight gain, energy intake, visceral adiposity and the level of serum triglycerides. It is of note that better metabolic profile was observed with FRG than RG for lipid metabolism and inflammation, in the liver in particular. Taken together, we demonstrated that RG and FRG supplementation effectively protected from HF-induced metabolic disturbances by improving obese phenotypes, lipid and inflammatory profiles, and antioxidant defense system.

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