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Quinoa Ameliorates Hepatic Steatosis, Oxidative Stress, Inflammation and Regulates the Gut Microbiota in Nonalcoholic Fatty Liver Disease Rats

A long-term high-fat diet causes hepatic steatosis, which further leads to oxidative stress and inflammation. In this study, we firstly investigated the regulation effects of different amounts of quinoa on hepatic steatosis, oxidative stress, and inflammation of rats fed a high-fat diet, then the gu...

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Published in:Foods 2023-04, Vol.12 (9), p.1780
Main Authors: Zhong, Lingyue, Lyu, Wei, Lin, Zihan, Lu, Jun, Geng, Yanlou, Song, Lihua, Zhang, Heng
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Lin, Zihan
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description A long-term high-fat diet causes hepatic steatosis, which further leads to oxidative stress and inflammation. In this study, we firstly investigated the regulation effects of different amounts of quinoa on hepatic steatosis, oxidative stress, and inflammation of rats fed a high-fat diet, then the gut microbiota was dynamically determined. Sprague-Dawley (SD, male) rats were randomized into four groups: normal controls (NC, fed standard chow), model groups (HF, fed a high-fat diet), low quinoa intake (HF + LQ), and high quinoa intake (HF + HQ) groups, which were supplemented with 9% and 27% quinoa in the high-fat feed (equivalent to 100 g/day and 300 g/day human intake, respectively). The results showed that quinoa intake significantly inhibited the hepatomegaly and splenomegaly, ameliorated hepatic steatosis pathologically; effectively rescued the decrease in the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) and the increase in malondialdehyde (MDA). The levels of tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), transforming growth factor-β (TGF-β), and leptin in rats of two quinoa groups were close to those of the NC group. Besides, high quinoa intake significantly increased the relative abundance of , and low quinoa intake significantly increased the relative abundance of at the genus level. The relative abundances of and in rats in the HF + HQ group were lower than those in rats in the HF + LQ group. In addition, the relative abundances of and of rats in the two quinoa intervention groups were lower than those of rats in the HF group after 12 weeks of intervention. In summary, quinoa exhibits a series of beneficial effects in the prevention of nonalcoholic fatty liver disease (NAFLD) and is suggested to be a component of a daily diet for the prevention of NAFLD.
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In this study, we firstly investigated the regulation effects of different amounts of quinoa on hepatic steatosis, oxidative stress, and inflammation of rats fed a high-fat diet, then the gut microbiota was dynamically determined. Sprague-Dawley (SD, male) rats were randomized into four groups: normal controls (NC, fed standard chow), model groups (HF, fed a high-fat diet), low quinoa intake (HF + LQ), and high quinoa intake (HF + HQ) groups, which were supplemented with 9% and 27% quinoa in the high-fat feed (equivalent to 100 g/day and 300 g/day human intake, respectively). The results showed that quinoa intake significantly inhibited the hepatomegaly and splenomegaly, ameliorated hepatic steatosis pathologically; effectively rescued the decrease in the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) and the increase in malondialdehyde (MDA). The levels of tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), transforming growth factor-β (TGF-β), and leptin in rats of two quinoa groups were close to those of the NC group. Besides, high quinoa intake significantly increased the relative abundance of , and low quinoa intake significantly increased the relative abundance of at the genus level. The relative abundances of and in rats in the HF + HQ group were lower than those in rats in the HF + LQ group. In addition, the relative abundances of and of rats in the two quinoa intervention groups were lower than those of rats in the HF group after 12 weeks of intervention. 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In this study, we firstly investigated the regulation effects of different amounts of quinoa on hepatic steatosis, oxidative stress, and inflammation of rats fed a high-fat diet, then the gut microbiota was dynamically determined. Sprague-Dawley (SD, male) rats were randomized into four groups: normal controls (NC, fed standard chow), model groups (HF, fed a high-fat diet), low quinoa intake (HF + LQ), and high quinoa intake (HF + HQ) groups, which were supplemented with 9% and 27% quinoa in the high-fat feed (equivalent to 100 g/day and 300 g/day human intake, respectively). The results showed that quinoa intake significantly inhibited the hepatomegaly and splenomegaly, ameliorated hepatic steatosis pathologically; effectively rescued the decrease in the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) and the increase in malondialdehyde (MDA). The levels of tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), transforming growth factor-β (TGF-β), and leptin in rats of two quinoa groups were close to those of the NC group. Besides, high quinoa intake significantly increased the relative abundance of , and low quinoa intake significantly increased the relative abundance of at the genus level. The relative abundances of and in rats in the HF + HQ group were lower than those in rats in the HF + LQ group. In addition, the relative abundances of and of rats in the two quinoa intervention groups were lower than those of rats in the HF group after 12 weeks of intervention. 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subjects Blautia
Body fat
Cholesterol
Diet
Fatty acids
Fatty liver
Feeds
Food science
Glutathione
Glutathione peroxidase
Growth factors
gut microbiota
High fat diet
Inflammation
Interleukin 10
Interleukins
Intestinal microflora
Laboratory animals
Leptin
Lipids
Liver
Liver diseases
Low fat diet
Microbiota
Microbiota (Symbiotic organisms)
Microorganisms
NAFLD
Nutrient deficiency
Oxidative stress
Peroxidase
Prevention
Quinoa
quinoa intake
Relative abundance
Spleen
Splenomegaly
Steatosis
Superoxide
Superoxide dismutase
Transforming growth factor-b
Transforming growth factors
Tumor necrosis factor-TNF
Tumor necrosis factor-α
title Quinoa Ameliorates Hepatic Steatosis, Oxidative Stress, Inflammation and Regulates the Gut Microbiota in Nonalcoholic Fatty Liver Disease Rats
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