Quinoa Reduces High-Fat Diet-Induced Obesity in Mice via Potential Microbiota-Gut-Brain-Liver Interaction Mechanisms

Wang, Tingye; Tao, Siyu; Wu, Yanxiang; An, Tian; Lv, Bohan; Liu, Jia-Xian; Liu, Yu-Tong; Jiang, Guiyan

doi:10.1128/spectrum.00329-22

Cited by 28 publications

(42 citation statements)

References 55 publications

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“…Additional studies have demonstrated that TUDCA can reduce ER stress by stimulating the TGR5 signaling pathway ( 108 , 109 ). It has been shown that upregulation of TGR5 expression inhibits the TLR4/NF-κB pathway to reduce oxidative stress, which may delay endothelial injury ( 85 ). TGR5 may alleviate ER stress through the protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK)/eukaryotic initiation factor 2(eIF2)/NF-κB pathway and activating transcription factor 4-CCAAT-enhancer-binding protein homologous protein (ATF4-CHOP); therefore, these targets have the potential to be used for delaying necrosis of diabetic RMECs ( 104 ).…”

Section: Discussion and Future Perspectivesmentioning

confidence: 99%

“…Since the activation of the TGR5 receptor improves EC injury caused by mitochondrial injury, oxidative stress, inflammatory factors, and ER stress, it may play a role in delaying DR-induced ED. Therefore, the TGR5 receptor can be used as a new target to ameliorate DR. Quinoa can cause an upregulation of the expression of GLP-1 via increased expression levels of TGR5 and it may be useful in the treatment of DR ( 85 ). Therefore, it is possible that certain components in Chenopodium album may act as agonists of TGR5.…”

Section: Discussion and Future Perspectivesmentioning

confidence: 99%

“…This increase in inflammatory factors leads to retinopathy ( 83 ). Previous studies have demonstrated that activation of the TGR5 receptor can delay the production of IL-1, TNF-α, and other inflammatory factors by macrophages; it may also reduce the production of proinflammatory factors by inhibiting the Toll-like receptor (TLR)4/NK-κβ pathway and can play a role in inhibiting the phosphorylation of STAT3 ( 21 , 84 , 85 ). Among all inflammatory factors, TNF-α was first implicated in the progression of insulin resistance, as well as in abnormal glucose metabolism associated with T2DM.…”

Section: Tgr5 and Inflammationmentioning

confidence: 99%

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Role of Takeda G protein‑coupled receptor 5 in microvascular endothelial cell dysfunction in diabetic retinopathy (Review)

Zhang

Dong

et al. 2022

Exp Ther Med

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Diabetic retinopathy (DR) is a frequent microvascular complication of advanced-stage diabetes. Endothelial cell dysfunction (ED) induced by diabetes plays an important role in the development of DR. It is considered that inflammation and mitochondrial homeostasis are associated with the progression of ED. Takeda G protein-coupled receptor 5 (TGR5) is a membrane receptor for bile acids (BAs) that plays an important role in regulating BA metabolism. Recent studies have shown that TGR5 is involved in regulating various mediators of ED and improving the dysfunction of vascular endothelial cells in DR; however, the exploration of specific related mechanisms remains an active research area in this field, which suggests that TGR5 may be one of the potential targets for the treatment of associated ED in DR. In the present review, the association between TGR5 and mitochondrial homeostasis was investigated. The extent of inflammation in DR-induced ED was assessed to provide possible evidence for the development of targeted therapies against DR.

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Section: Discussion and Future Perspectivesmentioning

confidence: 99%

Section: Discussion and Future Perspectivesmentioning

confidence: 99%

Section: Tgr5 and Inflammationmentioning

confidence: 99%

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Role of Takeda G protein‑coupled receptor 5 in microvascular endothelial cell dysfunction in diabetic retinopathy (Review)

Zhang

Dong

et al. 2022

Exp Ther Med

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“…The gut, brain, and liver interact closely with each other. For example, intestinal signals can activate the hypothalamic lipid-sensitive signals via the vagal afferent nerves, which in turn controls food intake ( 65 ). Simultaneously, the brain inhibits hepatic glucose production to suppress the onset of obesity.…”

Section: Link Between Microbiota and Non-alcoholic Fatty Liver Diseas...mentioning

confidence: 99%

Gut microbiota–mitochondrial inter-talk in non-alcoholic fatty liver disease

et al. 2022

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The increasing prevalence of non-alcoholic fatty liver disease (NAFLD), which is a progressive disease, has exerted huge a healthcare burden worldwide. New investigations have suggested that the gut microbiota closely participates in the progression of NAFLD through the gut–liver axis or gut–brain–liver axis. The composition of the microbiota can be altered by multiple factors, primarily dietary style, nutritional supplements, or exercise. Recent evidence has revealed that gut microbiota is involved in mitochondrial biogenesis and energy metabolism in the liver by regulating crucial transcription factors, enzymes, or genes. Moreover, microbiota metabolites can also affect mitochondrial oxidative stress function and swallow formation, subsequently controlling the inflammatory response and regulating the levels of inflammatory cytokines, which are the predominant regulators of NAFLD. This review focuses on the changes in the composition of the gut microbiota and metabolites as well as the cross-talk between gut microbiota and mitochondrial function. We thus aim to comprehensively explore the potential mechanisms of gut microbiota in NAFLD and potential therapeutic strategies targeting NAFLD management.

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“…In addition, gut bacterial secreted OGAs could protect rodents from ulcerative colitis by hydrolyzing O-GlcNAcylated proteins in the host ( He et al, 2021 ). According to current studies, gut microbiota might affect the level of intracerebral O-GlcNAc through short-chain fatty acids (SCFAs), bile acids, and gut-brain-liver interaction ( Cuervo-Zanatta et al, 2022 ; Hurley et al, 2022 ; Wang T. Y. et al, 2022 ). These studies revealed that in addition to being regulated by the host‘s hydrolase and transferase, the O-GlcNAcylated proteins in the host might be also controlled by bacterial-secreted OGTs and OGAs.…”

Section: Introductionmentioning

confidence: 99%

Liuwei Dihuang formula ameliorates chronic stress-induced emotional and cognitive impairments in mice by elevating hippocampal O-GlcNAc modification

Huang

Wang²,

Liu³

et al. 2023

Front. Neurosci.

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A substantial body of evidence has indicated that intracerebral O-linked N-acetyl-β-D-glucosamine (O-GlcNAc), a generalized post-translational modification, was emerging as an effective regulator of stress-induced emotional and cognitive impairments. Our previous studies showed that the Liuwei Dihuang formula (LW) significantly improved the emotional and cognitive dysfunctions in various types of stress mouse models. In the current study, we sought to determine the effects of LW on intracerebral O-GlcNAc levels in chronic unpredictable mild stress (CUMS) mice. The dynamic behavioral tests showed that anxiety- and depression-like behaviors and object recognition memory of CUMS mice were improved in a dose-dependent manner after LW treatment. Moreover, linear discriminate analysis (LEfSe) of genera abundance revealed a significant difference in microbiome among the study groups. LW showed a great impact on the relative abundance of these gut microbiota in CUMS mice and reinstated them to control mouse levels. We found that LW potentially altered the Uridine diphosphate-N-acetylglucosamine (UDP-GlcNAc) biosynthesis process, and the abundance of O-GlcNAcase (OGA) and O-GlcNAc transferase (OGT) in CUMS mice, which was inferred using PICRUSt analysis. We further verified advantageous changes in hippocampal O-GlcNAc modification of CUMS mice following LW administration, as well as changes in the levels of OGA and OGT. In summary, LW intervention increased the levels of hippocampal O-GlcNAc modification and ameliorated the emotional and cognitive impairments induced by chronic stress in CUMS mice. LW therefore could be considered a potential prophylactic and therapeutic agent for chronic stress.

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Quinoa Reduces High-Fat Diet-Induced Obesity in Mice via Potential Microbiota-Gut-Brain-Liver Interaction Mechanisms

Abstract: Gut microbiota has been investigated extensively, as a driver of obesity as well as a therapeutic target. Studies of its mechanisms are predominantly microbiota-gut-brain axis or microbiota-gut-liver axis.

Cited by 28 publications

References 55 publications

Role of Takeda G protein‑coupled receptor 5 in microvascular endothelial cell dysfunction in diabetic retinopathy (Review)

Role of Takeda G protein‑coupled receptor 5 in microvascular endothelial cell dysfunction in diabetic retinopathy (Review)

Gut microbiota–mitochondrial inter-talk in non-alcoholic fatty liver disease

Liuwei Dihuang formula ameliorates chronic stress-induced emotional and cognitive impairments in mice by elevating hippocampal O-GlcNAc modification

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