Alleviating the effect of quinoa and the underlying mechanism on hepatic steatosis in high-fat diet-fed rats

Abstract Background Nonalcoholic fatty liver disease (NAFLD) is considered the hepatic component of metabolic syndrome and has attracted widespread attention due to its increased prevalence. Daily dietary management is an effective strategy for the prevention of NAFLD. Quinoa, a nutritious pseudocereal, is abundant in antioxidative bioactive phytochemicals. In the present study, the effects of different amounts of quinoa on the progression of NAFLD and the related molecular mechanism were investigated. Methods Male SD rats were simultaneously administered a high fat diet (HF) and different amounts of quinoa (equivalent to 100 g/day and 300 g/day of human intake, respectively). After 12 weeks of the intervention, hepatic TG (triglyceride) and TC (total cholesterol) as well as serum antioxidative parameters were determined, and hematoxylin–eosin staining (H&E) staining was used to evaluate hepatic steatosis. Differential metabolites in serum and hepatic tissue were identified using UPLC-QTOF-MSE. The mRNA expression profile was investigated using RNA-Seq and further verified using real-time polymerase chain reaction (RT-PCR). Results Low amounts of quinoa (equivalent to 100 g/d of human intake) effectively controlled the weight of rats fed a high-fat diet. In addition, quinoa effectively inhibited the increase in hepatic TG and TC levels, mitigated pathological injury, promoted the increase in SOD and GSH-Px activities, and decreased MDA levels. Nontarget metabolic profile analysis showed that quinoa regulated lipid metabolites in the circulation system and liver such as LysoPC and PC. RNA-Seq and RT-PCR verification revealed that a high amount of quinoa more effectively upregulated genes related to lipid metabolism [Apoa (apolipoprotein)5, Apoa4, Apoc2] and downregulated genes related to the immune response [lrf (interferon regulatory factor)5, Tlr6 (Toll-like receptor), Tlr10, Tlr11, Tlr12]. Conclusion Quinoa effectively prevented NAFLD by controlling body weight, mitigating oxidative stress, and regulating the lipid metabolic profile and the expression of genes related to lipid metabolism and the immune response.

Download Full-text

Alleviating Effect of Quinoa and Underlying Mechanism on Hepatic Steatosis in High Fat Diet Fed Rat

10.21203/rs.3.rs-934267/v1 ◽

2021 ◽

Author(s):

Chenwei Song ◽

Wei Lv ◽

Yahui Li ◽

Pan Nie ◽

Jun Lu ◽

...

Keyword(s):

Immune Response ◽

Lipid Metabolism ◽

Fatty Liver ◽

Hepatic Steatosis ◽

Hepatic Tissue ◽

Circulation System ◽

Rna Seq ◽

Rt Pcr ◽

Alcoholic Fatty Liver ◽

The Metabolic Syndrome

Abstract Background: HF diet-associated fatty liver (is also known as non-alcoholic fatty liver disease, NAFLD) is considered the hepatic component of the metabolic syndrome and has attracted widespread attention due to the increase in its prevalence. Daily dietary management, is considered to be one of the effective strategies for the prevention of NAFLD. In the present study, the effect of quinoa on the hepatic steatosis and the metabolism mechanism were investigated.Methods: Male SD rats simultaneously administered an HF diet and different amounts of quinoa (equivalent to 100 g/day and 300 g/day of human intake, respectively). After 12 weeks of the intervention, Hepatic TG and TC as well as serum anti-oxidative parameters were determined, H&E staining evaluated the hepatic steatosis. Differential metabolite in serum and hepatic tissue were analyzed using UPLC-QTOF-MSE. mRNA expression profile were investigated using RNA-Seq and further verified using real-time RT-PCR.Results: It showed that quinoa effectively controlled the weight of rats, mitigated hepatic steatosis and oxidative stress, which exhibited the beneficial effect of quinoa on prevention of NAFLD. These beneficial effects could be attributed to the regulation of the production of certain metabolites in the circulation system or liver such as LysoPC and PC. The RNA-Seq analysis and RT-PCR verification revealed that an intake of a high amount of quinoa more effectively up-regulated the genes related to lipid metabolism [Apoa (apolipoprotein)5, Apoa4, Apoc2) and down-regulated the genes related immune response [lrf (interferon regulatory factor)5, Tlr6 (Toll like receptor), Tlr10, Tlr11, Tlr12]. Conclusions: Quinoa could alleviate hepatic steatosis due to the regulation of metabolism and the expression of genes related with lipid metabolism and immune response.

Download Full-text

Black rice anthocyanins alleviate hyperlipidemia, liver steatosis and insulin resistance by regulating lipid metabolism and gut microbiota in obese mice

Food & Function ◽

10.1039/d1fo01394g ◽

2021 ◽

Author(s):

Haizhao Song ◽

Xinchun Shen ◽

Yang Zhou ◽

Xiaodong Zheng

Keyword(s):

Insulin Resistance ◽

Lipid Metabolism ◽

Gut Microbiota ◽

Hepatic Steatosis ◽

High Fat Diet ◽

Liver Steatosis ◽

Obese Mice ◽

Black Rice ◽

High Fat ◽

Diet Induced Obesity

Supplementation of black rice anthocyanins (BRAN) alleviated high fat diet-induced obesity, insulin resistance and hepatic steatosis by improvement of lipid metabolism and modification of the gut microbiota.

Download Full-text

Fisetin Protects Against Hepatic Steatosis Through Regulation of the Sirt1/AMPK and Fatty Acid β-Oxidation Signaling Pathway in High-Fat Diet-Induced Obese Mice

Cellular Physiology and Biochemistry ◽

10.1159/000493650 ◽

2018 ◽

Vol 49 (5) ◽

pp. 1870-1884 ◽

Cited By ~ 25

Author(s):

Chian-Jiun Liou ◽

Ciao-Han Wei ◽

Ya-Ling Chen ◽

Ching-Yi Cheng ◽

Chia-Ling Wang ◽

...

Keyword(s):

Fatty Acid ◽

Lipid Metabolism ◽

Hepatic Steatosis ◽

Lipid Accumulation ◽

High Fat Diet ◽

Fatty Acid Synthase ◽

Epididymal Adipose Tissue ◽

Obese Mice ◽

High Fat

Background/Aims: Fisetin is a naturally abundant flavonoid isolated from various fruits and vegetables that was recently identified to have potential biological functions in improving allergic airway inflammation, as well as anti-oxidative and anti-tumor properties. Fisetin has also been demonstrated to have anti-obesity properties in mice. However, the effect of fisetin on nonalcoholic fatty liver disease (NAFLD) is still elusive. Thus, the present study evaluated whether fisetin improves hepatic steatosis in high-fat diet (HFD)-induced obese mice and regulates lipid metabolism of FL83B hepatocytes in vitro. Methods: NAFLD was induced by HFD in male C57BL/6 mice. The mice were then injected intraperitoneally with fisetin for 10 weeks. In another experiment, FL83B cells were challenged with oleic acid to induce lipid accumulation and treated with various concentrations of fisetin. Results: NAFLD mice treated with fisetin had decreased body weight and epididymal adipose tissue weight compared to NAFLD mice. Fisetin treatment also reduced liver lipid droplet and hepatocyte steatosis, alleviated serum free fatty acid, and leptin concentrations, significantly decreased fatty acid synthase, and significantly increased phosphorylation of AMPKα and the production of sirt-1 and carnitine palmitoyltransferase I in the liver tissue. In vitro, fisetin decreased lipid accumulation and increased lipolysis and β-oxidation in hepatocytes. Conclusion: This study suggests that fisetin is a potential novel treatment for alleviating hepatic lipid metabolism and improving NAFLD in mice via activation of the sirt1/AMPK and β-oxidation pathway.

Download Full-text

Vitamin D attenuates high fat diet-induced hepatic steatosis in rats by modulating lipid metabolism

European Journal of Clinical Investigation ◽

10.1111/j.1365-2362.2012.02706.x ◽

2012 ◽

Vol 42 (11) ◽

pp. 1189-1196 ◽

Cited By ~ 61

Author(s):

Yi Yin ◽

Zhiwen Yu ◽

Min Xia ◽

Xiaoqin Luo ◽

Xiaofei Lu ◽

...

Keyword(s):

Vitamin D ◽

Lipid Metabolism ◽

Hepatic Steatosis ◽

High Fat Diet ◽

High Fat

Download Full-text

CTRP3 attenuates diet-induced hepatic steatosis by regulating triglyceride metabolism

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00102.2013 ◽

2013 ◽

Vol 305 (3) ◽

pp. G214-G224 ◽

Cited By ~ 70

Author(s):

Jonathan M. Peterson ◽

Marcus M. Seldin ◽

Zhikui Wei ◽

Susan Aja ◽

G. William Wong

Keyword(s):

Lipid Metabolism ◽

Hepatic Steatosis ◽

High Fat Diet ◽

Therapeutic Potential ◽

Hepatic Triglyceride ◽

Wild Type ◽

High Fat ◽

Triglyceride Synthesis ◽

Modest Improvement ◽

Protective Function

CTRP3 is a secreted plasma protein of the C1q family that helps regulate hepatic gluconeogenesis and is downregulated in a diet-induced obese state. However, the role of CTRP3 in regulating lipid metabolism has not been established. Here, we used a transgenic mouse model to address the potential function of CTRP3 in ameliorating high-fat diet-induced metabolic stress. Both transgenic and wild-type mice fed a high-fat diet showed similar body weight gain, food intake, and energy expenditure. Despite similar adiposity to wild-type mice upon diet-induced obesity (DIO), CTRP3 transgenic mice were strikingly resistant to the development of hepatic steatosis, had reduced serum TNF-α levels, and demonstrated a modest improvement in systemic insulin sensitivity. Additionally, reduced hepatic triglyceride levels were due to decreased expression of enzymes (GPAT, AGPAT, and DGAT) involved in triglyceride synthesis. Importantly, short-term daily administration of recombinant CTRP3 to DIO mice for 5 days was sufficient to improve the fatty liver phenotype, evident as reduced hepatic triglyceride content and expression of triglyceride synthesis genes. Consistent with a direct effect on liver cells, recombinant CTRP3 treatment reduced fatty acid synthesis and neutral lipid accumulation in cultured rat H4IIE hepatocytes. Together, these results establish a novel role for CTRP3 hormone in regulating hepatic lipid metabolism and highlight its protective function and therapeutic potential in attenuating hepatic steatosis.

Download Full-text

Hepatic Steatosis as a Result of Altered Lipid Metabolism in Mice with Adipocyte-specific Fatp4-deficiency under High-fat Diet

Zeitschrift für Gastroenterologie ◽

10.1055/s-0030-1269568 ◽

2011 ◽

Vol 49 (01) ◽

Author(s):

LS Lenz ◽

J Marx ◽

W Chamulitrat ◽

I Kaiser ◽

HJ Gröne ◽

...

Keyword(s):

Lipid Metabolism ◽

Hepatic Steatosis ◽

High Fat Diet ◽

High Fat ◽

Altered Lipid Metabolism ◽

Altered Lipid

Download Full-text

Lactoferrin attenuates high-fat diet-induced hepatic steatosis and lipid metabolic dysfunctions by suppressing hepatic lipogenesis and down-regulating inflammation in C57BL/6J mice

Food & Function ◽

10.1039/c8fo00317c ◽

2018 ◽

Vol 9 (8) ◽

pp. 4328-4339 ◽

Cited By ~ 7

Author(s):

Ling Xiong ◽

Fazheng Ren ◽

Jiayi Lv ◽

Hao Zhang ◽

Huiyuan Guo

Keyword(s):

Lipid Metabolism ◽

Hepatic Steatosis ◽

High Fat Diet ◽

Regulatory Mechanisms ◽

Hepatic Lipogenesis ◽

High Fat ◽

Metabolic Dysfunctions

Lactoferrin was reported to exert modulatory effects on lipid metabolism, but the regulatory mechanisms remain unclear.

Download Full-text

Mogroside V Protects against Hepatic Steatosis in Mice on a High-Fat Diet and LO2 Cells Treated with Free Fatty Acids via AMPK Activation

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2020/7826874 ◽

2020 ◽

Vol 2020 ◽

pp. 1-11

Author(s):

Linghuan Li ◽

Wanfang Zheng ◽

Can Wang ◽

Jiameng Qi ◽

Hanbing Li

Keyword(s):

Fatty Acids ◽

Fatty Acid ◽

Lipid Metabolism ◽

Free Fatty Acids ◽

Mrna Expression ◽

Hepatic Steatosis ◽

High Fat Diet ◽

De Novo ◽

Acid Oxidation ◽

High Fat

Previous studies presented various beneficial effects of mogrosides extract from Siraitia grosvenorii, which has been included in the list of Medicine Food Homology Species in China. Mogroside V (MV) is one of the main ingredients in mogrosides extract; however, whether and how MV improves impaired lipid metabolism in the liver remains to be elucidated. Herein, we investigated the therapeutic effects of mogroside V upon hepatic steatosis in vivo and in vitro and explored the underlying mechanisms. The results showed that MV significantly ameliorated hepatic steatosis in high-fat diet- (HFD-) fed mice. Furthermore, the increased protein expression of PPAR-γ, SREBP-1, and FASN and mRNA expression of pparg, srebp1, scd1, and fasn in the liver in HFD-fed mice, which contribute to de novo lipogenesis, were dose-dependently reversed by MV treatment. Meanwhile, MV counteracted the suppressed expression of PPAR-α and CPT-1A and mRNA expression of atgl, hsl, ppara, and cpt1a, thus increasing lipolysis and fatty acid oxidation. In addition, in free fatty acids- (FFAs-) incubated LO2 cells MV downregulated de novo lipogenesis and upregulated lipolysis and fatty acid oxidation, thereby attenuating lipid accumulation, which was significantly abrogated by treatment with Compound C, an inhibitor of AMP-activated protein kinase (AMPK). Taken together, these results suggested that MV exerted a pronounced effect upon improving hepatic steatosis through regulating the disequilibrium of lipid metabolism in the liver via an AMPK-dependent pathway, providing a potential lead compound candidate for preventing nonalcoholic fatty liver disease.

Download Full-text