Green tea extract protects against hepatic NFκB activation along the gut-liver axis in diet-induced obese mice with nonalcoholic steatohepatitis by reducing endotoxin and TLR4/MyD88 signaling

Li, Jinhui; Sasaki, Geoffrey Y.; Dey, Priyankar; Chitchumroonchokchai, Chureeporn; Labyk, Allison N.; McDonald, Joshua D.; Kim, Joshua B.; Bruno, Richard S.

doi:10.1016/j.jnutbio.2017.10.016

Cited by 46 publications

(38 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition to visible signs of obesity, green tea has also been reported to inhibit obesity-induced inflammation (38). In obese mice model of nonalcoholic steatohepatitis, the green tea intervention significantly reduces the expression levels of proinflammatory genes (TNFα, iNOS, monocyte chemotactic protein 1, MCP-1, myeloperoxidase, MPO) likely via limiting endotoxin translocation and TLR4/MyD88/NFκB activation along the gut-liver axis (39). In previous study, researchers showed that obesity-mediated lymphoid dysfunction is regulated by accumulation of inflammatory cells around the lymphatic vessels, and T-cell inflammatory response is a necessary condition to initiate this effect (40).…”

Section: Discussionmentioning

confidence: 99%

Antiobesity and anti-inflammation effects of Hakka stir-fried tea of different storage years on high-fat diet-induced obese mice model via activating the AMPK/ACC/CPT1 pathway

Lai

Sun

et al. 2020

Food & Nutrition Research

View full text Add to dashboard Cite

Background: As a typical representative of metabolic syndrome, obesity is also one of the extremely dangerous factors of cardiovascular diseases. Thus, the prevention and treatment of obesity has gradually become a global campaign. There have been many reports that green tea is effective in preventing obesity, but as a kind of green tea with regional characteristics, there have been no reports that Hakka stir-fried tea (HT) of different storage years has a weight loss effect. Aims: The aim was to investigate the effect of HT in diet-induced obese mice. Methods: The mice were divided into five groups as follows: the control group received normal diet; the obese model group received high-fat diet; and HT2003, HT2008, and HT2015 groups, after the induction of obesity via a high-fat diet, received HT of different storage years treatment for 6 weeks, respectively. Results: It was observed that HT decreased the levels of serum and liver triglyceride; the ratio of liver to body weight; accumulation of epididymal, perirenal, and mesenteric fat; the degree of hepatic steatosis; and adipocyte hypertrophy, with the concomitant reduction of body weight. Moreover, HT decreased the expression levels of proinflammatory cytokines tumor necrosis factor α (TNF α), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and reduced fatty acid synthase (FAS) activity in liver tissue of obese mice. In addition, HT treatment also increased the phosphorylation of AMP-activated protein kinase (AMPK) and its direct downstream proteins, acetyl coenzyme A carboxylase (ACC), and carnitine palmitoyltransferase I (CPT-1), which participate in FAS pathway. Conclusions: These findings demonstrate that HT treatment has a potential protection on high-fat diet-induced obesity mice via activating the AMPK/ACC/CPT1 pathway, and to a certain extent, it has nothing to do with the storage time of three kinds of HT.

show abstract

Section: Discussionmentioning

confidence: 99%

Antiobesity and anti-inflammation effects of Hakka stir-fried tea of different storage years on high-fat diet-induced obese mice model via activating the AMPK/ACC/CPT1 pathway

Lai

Sun

et al. 2020

Food & Nutrition Research

View full text Add to dashboard Cite

show abstract

“…This chylomicron-dependent mechanism protects against TLR4-induced inflammation by directing LPS to the lymphatics instead of the portal stream, sequestering LPS away from circulating white cells by instead delivering it to the liver for detoxification [32]. However, increased LPS absorption is promoted by a high-fat diet that not only increases chylomicron secretion, but also increases gut barrier dysfunction, thereby allowing LPS passage and increasing circulating LPS, which potentiates endotoxemia-associated inflammation [13], [33], [34], [35].…”

Section: Why Would Improved Vitamin C Status Decrease Endotoxemia In mentioning

confidence: 99%

The relationship between vitamin C status, the gut-liver axis, and metabolic syndrome

2019

Self Cite

View full text Add to dashboard Cite

Metabolic syndrome (MetS) is a constellation of cardiometabolic risk factors, which together predict increased risk of more serious chronic diseases. We propose that one consequence of dietary overnutrition is increased abundance of Gram-negative bacteria in the gut that cause increased inflammation, impaired gut function, and endotoxemia that further dysregulate the already compromised antioxidant vitamin status in MetS. This discussion is timely because “healthy” individuals are no longer the societal norm and specialized dietary requirements are needed for the growing prevalence of MetS. Further, these lines of evidence provide the foundational basis for investigation that poor vitamin C status promotes endotoxemia, leading to metabolic dysfunction that impairs vitamin E trafficking through a mechanism involving the gut-liver axis. This report will establish a critical need for translational research aimed at validating therapeutic approaches to manage endotoxemia—an early, but inflammation-inducing phenomenon, which not only occurs in MetS, but is also prognostic of more advanced metabolic disorders including type 2 diabetes mellitus, as well as the increasing severity of nonalcoholic fatty liver diseases.

show abstract

“…Extensive research performed in recent years has revealed that EGCG exhibits a strong antioxidant capacity to mitigate the effects of heat stress on growth performance (Luo et al, ; Orhan et al, ) and meat quality (Huang, Zhang, Zhou, Wan, & Zhang, ; Zhang et al, ) in poultry. Green tea polyphenols and EGCG also blocked the nuclear factor‐kappa B (NF‐κB) pathway to inhibit pro‐inflammatory cytokine expression (Li et al, ; Orhan et al, ; Thichanpiang & Wongprasert, ). Therefore, we postulated that EGCG should alleviate the intestinal barrier breakdown and inflammatory disease induced by heat stress in poultry.…”

Section: Introductionmentioning

confidence: 99%

The effect of Epigallocatechin‐3‐gallate on small intestinal morphology, antioxidant capacity and anti‐inflammatory effect in heat‐stressed broilers

Song

Lei

Luo

et al. 2019

Animal Physiology Nutrition

View full text Add to dashboard Cite

This study was to investigate the effects of Epigallocatechin‐3‐gallate (EGCG) on intestinal morphology, antioxidant capacity and anti‐inflammatory response in heat‐stressed broiler. A total of 192 2‐week‐old Arbour Acres broilers chickens were divided into four groups with six replicates per group and eight chickens per replicate: one thermoneutral control group (28°C, group TN), which was fed the basal diet; and three cyclic high‐temperature groups (35°C from 7:00 to 19:00 hr; 28°C from 19:00 hr to 7:00 hr, heat stress group), which were fed the basal diet supplementation with EGCG 0 mg/kg (group HS0), 300 mg/kg (group HS300) and 600 mg/kg (group HS600). The gut morphology and intestinal mucosal oxidative stress indicators, as well as intestinal barrier‐related gene expression, were analysed. The results showed that compared with group TN, heat stress reduced the villus height (VH), activities of glutathione peroxidase (GSH‐Px), superoxide dismutase (SOD)and catalase (CAT), increased the crypt depth (CD) and malondialdehyde (MDA)content at 21, 28 and 35 days (p < 0.05). After the heat‐stressed broilers were supplemented with EGCG, VH, VH/CD (V/C), and the activities of GSH‐Px, SOD and CAT were increased, and CD and MDA content were reduced compared with those in group HS0 without EGCG supplementation at 21, 28 and 35 days (p < 0.05). The EGCG supplementation promoted the gene expression of nuclear factor‐erythroid 2‐related factor 2 (Nrf2), Claudin‐1, Mucin 2 (Muc2) and alleviated the nuclear factor‐kappa B (NF‐κB) and lipopolysaccharide‐induced tumour necrosis factor (LITAF) gene expression compared with group HS0 (p < 0.05). Moreover, intestinal morphology was strongly correlated with antioxidant ability and inflammatory response. In conclusion, EGCG alleviated the gut oxidative injury of heat‐stressed broilers by enhancing antioxidant capacity and inhibiting inflammatory response.

show abstract

Green tea extract protects against hepatic NFκB activation along the gut-liver axis in diet-induced obese mice with nonalcoholic steatohepatitis by reducing endotoxin and TLR4/MyD88 signaling

Cited by 46 publications

References 53 publications

Antiobesity and anti-inflammation effects of Hakka stir-fried tea of different storage years on high-fat diet-induced obese mice model via activating the AMPK/ACC/CPT1 pathway

Antiobesity and anti-inflammation effects of Hakka stir-fried tea of different storage years on high-fat diet-induced obese mice model via activating the AMPK/ACC/CPT1 pathway

The relationship between vitamin C status, the gut-liver axis, and metabolic syndrome

The effect of Epigallocatechin‐3‐gallate on small intestinal morphology, antioxidant capacity and anti‐inflammatory effect in heat‐stressed broilers

Contact Info

Product

Resources

About