Sargassum fusiforme Fucoidan Alleviates High-Fat Diet-Induced Obesity and Insulin Resistance Associated with the Improvement of Hepatic Oxidative Stress and Gut Microbiota Profile

2020 ◽  
Vol 68 (39) ◽  
pp. 10626-10638
Author(s):  
Ya Zhang ◽  
Jihui Zuo ◽  
Liping Yan ◽  
Yang Cheng ◽  
Qiaojuan Li ◽  
...  
2021 ◽  
Author(s):  
Haizhao Song ◽  
Xinchun Shen ◽  
Yang Zhou ◽  
Xiaodong Zheng

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.


2020 ◽  
Vol 11 (4) ◽  
pp. 2953-2968 ◽  
Author(s):  
Xiaobing Yang ◽  
Wenjing Mo ◽  
Chuanjin Zheng ◽  
Wenzhi Li ◽  
Jian Tang ◽  
...  

Non-alcoholic fatty liver disease is associated with gut microbiota, oxidative stress, and inflammation.


Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1289
Author(s):  
Anna Maria Giudetti ◽  
Daniele Vergara ◽  
Serena Longo ◽  
Marzia Friuli ◽  
Barbara Eramo ◽  
...  

Long-term high-fat diet (HFD) consumption can cause weight gain and obesity, two conditions often associated with hepatic non-alcoholic fatty liver and oxidative stress. Oleoylethanolamide (OEA), a lipid compound produced by the intestine from oleic acid, has been associated with different beneficial effects in diet-induced obesity and hepatic steatosis. However, the role of OEA on hepatic oxidative stress has not been fully elucidated. In this study, we used a model of diet-induced obesity to study the possible antioxidant effect of OEA in the liver. In this model rats with free access to an HFD for 77 days developed obesity, steatosis, and hepatic oxidative stress, as compared to rats consuming a low-fat diet for the same period. Several parameters associated with oxidative stress were then measured after two weeks of OEA administration to diet-induced obese rats. We showed that OEA reduced, compared to HFD-fed rats, obesity, steatosis, and the plasma level of triacylglycerols and transaminases. Moreover, OEA decreased the amount of malondialdehyde and carbonylated proteins and restored the activity of antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase, which decreased in the liver of HFD-fed rats. OEA had also an improving effect on parameters linked to endoplasmic reticulum stress, thus demonstrating a role in the homeostatic control of protein folding. Finally, we reported that OEA differently regulated the expression of two transcription factors involved in the control of lipid metabolism and antioxidant genes, namely nuclear factor erythroid-derived 2-related factor 1 (Nrf1) and Nrf2, thus suggesting, for the first time, new targets of the protective effect of OEA in the liver.


2018 ◽  
Vol 188 (1) ◽  
pp. 241-259 ◽  
Author(s):  
Mohamad Hafizi Abu Bakar ◽  
Mohamad Nurul Azmi ◽  
Khairul Anuar Shariff ◽  
Joo Shun Tan

2021 ◽  
Author(s):  
◽  
Ya Zhang

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disease characterized by hyperglycemia resulting from progressive loss of β-cell insulin secretion frequently on the background of insulin resistance. T2DM, also known as non-insulin-dependent diabetes, accounts for more than 90% of all cases of diabetes. Insulin resistance (IR) refers to the reduced sensitivity of peripheral tissues to insulin and is one of the important triggers of type 2 diabetes. Sargassum fusiforme polysaccharide exhibits diverse biological activities, and more and more studies have shown it has a significant effect in improving insulin resistance with almost no side effects. Sargassum fusiforme fucoidan (SFF) is one of the main active components with active ingredients such as antioxidants and hypoglycemic lipids. However, the ameliorative effects of SFF on high-fat diet-induced insulin resistance mice and its underlying physiological mechanisms are not clear. Hence, the polysaccharides were extracted and purified from Sargassum fusiforme, and fucoidan (SFF), which has good antioxidant activity, was screened using a drosophila melanogaster aging model. The effect of SFF on the amelioration of insulin resistance in mice was investigated with a high-fat obese insulin resistance mice model. By gut microbiota and metabolomics techniques, the effect of SFF on intestinal metabolites and its mechanism of alleviate IR were investigated. After treatment with 200 mg/kg SFF for 8 weeks, it was found that SFF could reduce body weight, fasting blood glucose and homa-IR in insulin resistance mice. SFF could effectively activate Nrf2/ARE antioxidant signaling pathway in the liver and promote Nrf2 entry into the nucleus and downstream gene transcription. Metabolomics and intestinal microecology revealed that SFF could upregulate TUDCA level and downregulate ceramide level in mice colon and serum, and this change was dependent on gut microbiota. TUDCA effectively inhibits the FXR/SHP signaling pathway activated by a high-fat diet, thereby reducing the biosynthesis of enteric-derived ceramides. In addition, TUDCA in the liver could compete with Nrf2 to bind Keap1 to reduce the formation of the Nrf2/Keap1 complex, reduce Nrf2 ubiquitination, and thus contribute to Nrf2/ARE signaling activation. In conclusion, fucoidan from S. fusiforme was able to modulate gut microbiota, increased the levels of the intestinal metabolite TUDCA, reduced biosynthesis of entericderived ceramides and activated the Nrf2/ARE pathway, which in turn significantly improved insulin resistance induced by high-fat diet in mice. This study provides a new research idea for the study of brown algae fucoidan in metabolic diseases.


Antioxidants ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 640
Author(s):  
Adriana Ortega-Hernández ◽  
Ernesto Martínez-Martínez ◽  
Ruben Gómez-Gordo ◽  
Natalia López-Andrés ◽  
Amaya Fernández-Celis ◽  
...  

Background: The objective of this study is to determine the role of mitochondrial oxidative stress in the dysbiosis associated with a high fat diet in rats. In addition, the impact of gut microbiota (GM) in the cardiometabolic consequences of diet-induced obesity in rats has been evaluated. Methods: Male Wistar rats were fed either a high fat diet (HFD) or a control (CT) one for 6 weeks. At the third week, one-half of the animals of each group were treated with the mitochondrial antioxidant MitoTempo (MT; 0.7 mgKg−1day−1 i.p). Results: Animals fed an HFD showed a lower microbiota evenness and diversity in comparison to CT rats. This dysbiosis is characterized by a decrease in Firmicutes/Bacteroidetes ratio and relevant changes at family and genera compared with the CT group. This was accompanied by a reduction in colonic mucin-secreting goblet cells. These changes were reversed by MT treatment. The abundance of certain genera could also be relevant in the metabolic consequences of obesity, as well as in the occurrence of cardiac fibrosis associated with obesity. Conclusions: These results support an interaction between GM and mitochondrial oxidative stress and its relation with development of cardiac fibrosis, suggesting new approaches in the management of obesity-related cardiometabolic consequences.


2020 ◽  
Author(s):  
Ya Zhang ◽  
Yang Cheng ◽  
Jihui Zuo ◽  
Liping Yan ◽  
Qiaojuan Li ◽  
...  

AbstractMetformin is widely used to surmount insulin resistance (IR) and diabetes. Evidence indicates that metformin remodels gut microbiota but the underlying mechanism remain unclear. Present results showed that metformin effectively improved insulin sensitivity and alleviated liver inflammation and oxidative stress in high fat diet (HFD)-induced mice. Metabolomics analysis showed that metformin increased tauroursodeoxycholic acid (TUDCA) production by increasing the expression of bile acid synthase Cyp7a1 and Baat. In the palmitic acid (PA)-induced cell, TUDCA activated Nrf2/ARE pathway, thereby reducing intracellular ROS and improving insulin signaling. Further gut microbiota analysis showed that metformin increased the proportion of Akkermanisia muciniphlia in the HFD-fed mice, while TUDCA promoted the proliferation of A. muciniphlia but metformin did not. These findings reveal that metformin remodels the gut microbiota, reduces oxidative stress and enhances insulin sensitivity by increasing the production of TUDCA. This provides a novel mechanism by which metformin alleviates diet-induced IR and improves metabolism.


2013 ◽  
Author(s):  
Maya Ramdas ◽  
Chava Harel ◽  
Natalia Krits ◽  
Michal Armoni ◽  
Eddy Karnieli

iScience ◽  
2021 ◽  
Vol 24 (2) ◽  
pp. 102077
Author(s):  
Hu Hua ◽  
Yue Zhang ◽  
Fei Zhao ◽  
Ke Chen ◽  
Tong Wu ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document