scholarly journals The phytochemical epigallocatechin gallate prolongs the lifespan by improving lipid metabolism, reducing inflammation and oxidative stress in high‐fat diet‐fed obese rats

Aging Cell ◽  
2020 ◽  
Vol 19 (9) ◽  
Author(s):  
Hang Yuan ◽  
Yuqiao Li ◽  
Fan Ling ◽  
Yue Guan ◽  
Dandan Zhang ◽  
...  
2010 ◽  
Vol 121 (4) ◽  
pp. 1010-1013 ◽  
Author(s):  
Tuoping Li ◽  
Suhong Li ◽  
Lijuan Du ◽  
Na Wang ◽  
Mei Guo ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Shoumen Lasker ◽  
Md Mizanur Rahman ◽  
Faisal Parvez ◽  
Mushfera Zamila ◽  
Pintu Miah ◽  
...  

AbstractThe main objective of this experiment was to determine the effects of yogurt supplementation on fat deposition, oxidative stress, inflammation and fibrosis in the liver of rats with high-fat (HF) diet-induced obesity. Male Wistar rats were used in this study and were separated into the following four different groups: the control, control + yogurt, high fat and high fat+ yogurt groups. The high fat groups received a HF diet for eight weeks. A 5% yogurt (w/w) supplement was also provided to rats fed the HF diet. Yogurt supplementation prevented glucose intolerance and normalized liver-specific enzyme activities in the HF diet-fed rats. Yogurt supplementation also significantly reduced the levels of oxidative stress markers in the plasma and liver of HF diet-fed rats. Moreover, inflammatory cell infiltration, collagen deposition and fibrosis in the liver of HF diet-fed rats were also prevented by yogurt supplementation. Furthermore, yogurt supplementation normalized the intestinal lining and brush border in HF diet-fed rats. This study suggests that yogurt supplementation potentially represents an alternative therapy for the prevention of metabolic syndrome in HF diet-fed rats.


2019 ◽  
Vol 58 ◽  
pp. 282-291 ◽  
Author(s):  
Andressa Rodrigues de Sousa ◽  
Maria Eliza de Castro Moreira ◽  
Mariana Grancieri ◽  
Renata Celi Lopes Toledo ◽  
Fernanda de Oliveira Araújo ◽  
...  

2014 ◽  
Vol 112 (4) ◽  
pp. 477-485 ◽  
Author(s):  
Xiaowei Sun ◽  
Rennan Feng ◽  
Yanchuan Li ◽  
Song Lin ◽  
Wei Zhang ◽  
...  

Obesity is considered to be accompanied by a chronic low-grade inflammatory state that contributes to the occurrence of many chronic diseases. Our previous study has demonstrated that histidine supplementation significantly ameliorates inflammation and oxidative stress in obese women. However, the in vivo potential mechanisms are not known. The present study was conducted to investigate the mechanisms underlying the effects of histidine on inflammation in a high-fat diet (HFD)-induced female obese rat model. An obese model was established in female Sprague–Dawley rats by HFD feeding for 8 weeks and followed by histidine supplementation for another 4 weeks. The results revealed that HFD-increased body weight and HFD-lowered serum histidine concentrations were significantly reversed by histidine supplementation (P< 0·05). In addition, the serum concentrations of TNF-α, IL-6, C-reactive protein (CRP) and malondialdehyde were significantly reduced and those of superoxide dismutase (SOD) were significantly increased by histidine supplementation when compared with those in obese rats (P< 0·05). Correspondingly, the mRNA expressions of TNF-α, IL-6 and CRP in the adipose tissue were significantly down-regulated and that of CuZnSOD was significantly up-regulated by histidine supplementation (P< 0·05). Histidine supplementation significantly reduced the HFD-induced translocation of NF-κB p65 into the nucleus (P= 0·032) by reducing the phosphorylation of the inhibitor of κBα in the adipose tissue. The results also revealed that the expression of adiponectin was markedly increased both in the serum and in the adipose tissue after histidine supplementation, accompanied by the activation of PPARγ (P= 0·021). These findings indicate that histidine is an effective candidate for ameliorating inflammation and oxidative stress in obese individuals via the NF-κB- and PPARγ-involved pathways.


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