Curcumin prevents liver fat accumulation and serum fetuin-A increase in rats fed a high-fat diet

2013 ◽  
Vol 69 (4) ◽  
pp. 677-686 ◽  
Author(s):  
Yildiz Öner-İyidoğan ◽  
Hikmet Koçak ◽  
Muhammed Seyidhanoğlu ◽  
Figen Gürdöl ◽  
Ahmet Gülçubuk ◽  
...  
2019 ◽  
Vol 44 (3) ◽  
pp. 320-325 ◽  
Author(s):  
Hsin-Yi Yang ◽  
Wan-Ju Yeh ◽  
Jung Ko ◽  
Jiun-Rong Chen

The objective of this study was to evaluate the effects of the hot-water extract of defatted Camellia oleifera seeds (CSE) on body and liver fat accumulation in rats. Forty rats were divided into 5 groups and each group was fed either an isocaloric control diet or a high-fat liquid diet with 0% (H), 0.12% (H1), 0.24% (H2), or 0.48% CSE (H3) for 8 weeks. Ingestion of the high-fat liquid diet increased abdominal and liver fat accumulation, although no difference was found in body weights compared with rats fed the control diet. We found that rats fed the H2 and H3 diets had lower plasma alanine aminotransferase activities than the H group in the fourth and eighth weeks. At the end of the study, the H2 and H3 groups also had lower epididymal and retroperitoneal fat masses, and all CSE groups had lower circulatory leptin levels than the H group. CSE consumption decreased hepatic fat accumulation in terms of liver triglycerides and a histopathology analysis, and ameliorated high-fat diet-induced elevation of hepatic tumor necrosis factor-α levels. We also found that CSE groups had lower malondialdehyde and hydroxyproline levels in the liver. Our results suggested that CSE may exert beneficial effects through decreasing body fat accumulation and hepatic steatosis and regulating adipokine levels in diet-induced nonalcoholic fatty liver disease.


2020 ◽  
Vol 24 (4) ◽  
pp. 214-219
Author(s):  
Mi Kyung Shin ◽  
Soo-Man Yang ◽  
In-Seob Han

2011 ◽  
Vol 300 (1) ◽  
pp. E122-E133 ◽  
Author(s):  
Takatoshi Murase ◽  
Koichi Misawa ◽  
Yoshihiko Minegishi ◽  
Masafumi Aoki ◽  
Hideo Ominami ◽  
...  

The prevalence of obesity is increasing globally, and obesity is a major risk factor for type 2 diabetes and cardiovascular disease. We investigated the effects of coffee polyphenols (CPP), which are abundant in coffee and consumed worldwide, on diet-induced body fat accumulation. C57BL/6J mice were fed either a control diet, a high-fat diet, or a high-fat diet supplemented with 0.5 to 1.0% CPP for 2–15 wk. Supplementation with CPP significantly reduced body weight gain, abdominal and liver fat accumulation, and infiltration of macrophages into adipose tissues. Energy expenditure evaluated by indirect calorimetry was significantly increased in CPP-fed mice. The mRNA levels of sterol regulatory element-binding protein (SREBP)-1c, acetyl-CoA carboxylase-1 and -2, stearoyl-CoA desaturase-1, and pyruvate dehydrogenase kinase-4 in the liver were significantly lower in CPP-fed mice than in high-fat control mice. Similarly, CPP suppressed the expression of these molecules in Hepa 1–6 cells, concomitant with an increase in microRNA-122. Structure-activity relationship studies of nine quinic acid derivatives isolated from CPP in Hepa 1–6 cells suggested that mono- or di-caffeoyl quinic acids (CQA) are active substances in the beneficial effects of CPP. Furthermore, CPP and 5-CQA decreased the nuclear active form of SREBP-1, acetyl-CoA carboxylase activity, and cellular malonyl-CoA levels. These findings indicate that CPP enhances energy metabolism and reduces lipogenesis by downregulating SREBP-1c and related molecules, which leads to the suppression of body fat accumulation.


2016 ◽  
Vol 122 (2) ◽  
pp. 94-102 ◽  
Author(s):  
Muhammed Seyithanoğlu ◽  
Yıldız Öner-İyidoğan ◽  
Semra Doğru-Abbasoğlu ◽  
Sevda Tanrıkulu-Küçük ◽  
Hikmet Koçak ◽  
...  

2015 ◽  
Vol 12 (1) ◽  
Author(s):  
Siti N. Wulan ◽  
Vera B. Schrauwen-Hinderling ◽  
Klaas R. Westerterp ◽  
Guy Plasqui

2013 ◽  
Vol 305 (8) ◽  
pp. E987-E998 ◽  
Author(s):  
K. Tajima ◽  
A. Nakamura ◽  
J. Shirakawa ◽  
Y. Togashi ◽  
K. Orime ◽  
...  

The prevalence of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) is increasing with the growing epidemics of obesity and diabetes. NAFLD encompasses a clinicopathologic spectrum of disease ranging from isolated hepatic steatosis to NASH, which is a more aggressive form of fatty liver disease, to cirrhosis and, finally, hepatocellular carcinoma (HCC). The exact mechanism behind the development of HCC in NASH remains unclear; however, it has been established that hepatic steatosis is the important risk factor in the development of HCC. Metformin has recently drawn attention because of its potential antitumor effect. Here, we investigated the effects of metformin on high-fat diet (HFD)-induced liver tumorigenesis, using a mouse model of NASH and liver tumor. Metformin prevented long-term HFD-induced liver tumorigenesis in C57Bl/6 mice. Of note, metformin failed to protect against liver tumorigenesis in mice that had already begun to develop NAFLD. Metformin improved short-term HFD-induced fat accumulation in the liver, associated with the suppression of adipose tissue inflammation. Collectively, these results suggest that metformin may prevent liver tumorigenesis via suppression of liver fat accumulation in the early stage, before the onset of NAFLD, which seems to be associated with a delay in the development of inflammation of the adipose tissue.


2021 ◽  
Author(s):  
Yilin Liu ◽  
Chunyan Xie ◽  
Zhenya Zhai ◽  
Ze-yuan Deng ◽  
Hugo R. De Jonge ◽  
...  

This study aimed to investigate the effect of uridine on obesity, fat accumulation in liver, and gut microbiota composition in high-fat diet-fed mice.


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