Gut Microbiota: Association with NAFLD and Metabolic Disturbances

Lau, Eva; Carvalho, Davide; Freitas, Paula

doi:10.1155/2015/979515

Cited by 74 publications

(88 citation statements)

References 52 publications

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“…Intestinal microbiota composition modulates glucose homeostasis and hepatic lipid metabolism, contributing to NAFLD development as an environmental factor [29,66].…”

Section: Thus Quercetin Reduced the Increased Firmicutes/bacteroidetesmentioning

confidence: 99%

Protective effect of quercetin on high-fat diet-induced non-alcoholic fatty liver disease in mice is mediated by modulating intestinal microbiota imbalance and related gut-liver axis activation

Porras

Nistal

Martínez‐Flórez

et al. 2017

Free Radical Biology and Medicine

399

259

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Abbreviations: ALT, alanine aminotransferase; C/EBPα, CCAAT/enhancer binding protein alpha; CHOP, CCAAT-enhancer-binding protein homologous protein; CYP2E1, cytochrome P450 2E1; DAMPs, danger-associated molecular patterns; FABP1, fatty acid binding protein 1; FAS, fatty acid synthase; FAT/CD36, fatty acid translocase CD36; FFA, free fatty acid; FOXA1, forkhead box protein A1; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GRP78, 78 kDa glucose-regulated protein; HFD, high fat diet; HOMA-IR, homeostasis model assessment of insulin resistance; IAP, intestinal phosphatase alkaline; IL-6, interleukin 6; LPO, lipid peroxidation; LPS, lipopolysaccharide; LXRα, liver X receptor alpha; NAFLD, non-alcoholic fatty liver disease; NAS, NAFLD activity score; NASH, non-alcoholic steatohepatitis; NF-B , nuclear factor kappa B; NLRP3, NOD-like receptor family pyrin domain containing 3;PAMPs, pathogen-associated molecular patterns; PRRs, pattern recognition receptors; SCFAs, short-chain fatty acids; SREBP-1c, sterol regulatory element binding protein 1c; TG, triglycerides; TLR, Toll-like receptor; TNF-αtumor necrosis factor; UPR, unfolded protein response. AbstractGut microbiota is involved in obesity, metabolic syndrome and the progression of nonalcoholic fatty liver disease (NAFLD). It has been recently suggested that the flavonoid quercetin may have the ability to modulate the intestinal microbiota composition, suggesting a prebiotic capacity which highlights a great therapeutic potential in NAFLD. The present study aims to investigate benefits of experimental treatment with quercetin on gut microbial balance and related gut-liver axis activation in a nutritional animal model of NAFLD associated to obesity. C57BL/6J mice were challenged with high fat diet (HFD) supplemented or not with quercetin for 16 weeks.

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“…Intestinal microbiota composition modulates glucose homeostasis and hepatic lipid metabolism, contributing to NAFLD development as an environmental factor [29,66].…”

Section: Thus Quercetin Reduced the Increased Firmicutes/bacteroidetesmentioning

confidence: 99%

Protective effect of quercetin on high-fat diet-induced non-alcoholic fatty liver disease in mice is mediated by modulating intestinal microbiota imbalance and related gut-liver axis activation

Porras

Nistal

Martínez‐Flórez

et al. 2017

Free Radical Biology and Medicine

399

259

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“…Specifically, the gut microbiota can influence host metabolism through gut signaling pathways that affect insulin resistance, lipid metabolism, ethanol production, and inflammation (26, 29). The mechanisms by which the microbiota induce obesity include increasing gut permeability that causes bacterial translocation and increased hepatic and systemic inflammation, production of short-chain fatty acids (SCFAs), and greater extraction of energy from the diet (26,35).Little is known about the effect of aerobic fitness on the microbiome and its potential role in disease development. Therefore, we used the HCR/LCR rat model system to determine 1) whether intrinsic aerobic fitness affects the cecal microbiota; and 2) whether acute changes in the microbiota following 3 days of HFD feeding are associated with development of hepatic steatosis.…”

mentioning

confidence: 99%

Gut microbiota are linked to increased susceptibility to hepatic steatosis in low-aerobic-capacity rats fed an acute high-fat diet

Panasevich

Morris

Chintapalli

et al. 2016

American Journal of Physiology-Gastrointestinal and Liver Physi

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Panasevich MR, Morris EM, Chintapalli SV, Wankhade UD, Shankar K, Britton SL, Koch LG, Thyfault JP, Rector RS. Gut microbiota are linked to increased susceptibility to hepatic steatosis in low-aerobic-capacity rats fed an acute high-fat diet. Am J Physiol Gastrointest Liver Physiol 311: G166 -G179, 2016. First published June 10, 2016; doi:10.1152/ajpgi.00065.2016.-Poor aerobic fitness is linked to nonalcoholic fatty liver disease and increased all-cause mortality. We previously found that rats with a low capacity for running (LCR) that were fed an acute high-fat diet (HFD; 45% kcal from fat) for 3 days resulted in positive energy balance and increased hepatic steatosis compared with rats that were highly aerobically fit with a high capacity for running (HCR). Here, we tested the hypothesis that poor physiological outcomes in LCR rats following acute HFD feeding are associated with alterations in cecal microbiota. LCR rats exhibited greater body weight, feeding efficiency, 3 days of body weight change, and liver triglycerides after acute HFD feeding compared with HCR rats. Furthermore, compared with HCR rats, LCR rats exhibited reduced expression of intestinal tight junction proteins. Cecal bacterial 16S rDNA revealed that LCR rats had reduced cecal Proteobacteria compared with HCR rats. Microbiota of HCR rats consisted of greater relative abundance of Desulfovibrionaceae and unassigned genera within this family, suggesting increased reduction of endogenous mucins and proteins. Although feeding rats an acute HFD led to reduced Firmicutes in both strains, short-chain fatty acid-producing Phascolarctobacterium was reduced in LCR rats. In addition, Ruminococcae and Ruminococcus were negatively correlated with energy intake in the LCR/HFD rats. Predicted metagenomic function suggested that LCR rats had a greater capacity to metabolize carbohydrate and energy compared with HCR rats. Overall, these data suggest that the populations and metabolic capacity of the microbiota in low-aerobically fit LCR rats may contribute to their susceptibility to acute HFD-induced hepatic steatosis and poor physiologic outcomes. microbiota; short-chain fatty acids; aerobic fitness; NAFLD A SEDENTARY LIFESTYLE AND low aerobic fitness are strong independent risk factors for cardiovascular disease and allcause mortality (28). Nonalcoholic fatty liver disease (NAFLD) is becoming more prevalent and is increasing concomitant with the rise in obesity (51). Progression of the disease begins with simple hepatic steatosis, which in some individuals, may progress to more severe liver diseases (i.e., inflammation, fibrosis, and cirrhosis). Several studies have shown that low aerobic fitness and physical inactivity are inversely related to the development and progression of NA-FLD (10, 42, 44); however, the mechanisms explaining this link are poorly understood. We previously demonstrated that sedentary rats selectively bred for low-capacity running (LCR) fed an acute high-fat diet (HFD; 45% kcal from fat) for 3 days were more susceptible to developme...

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“…Barbara D et al reported that FOS supplement reduced hepatic triglyceride accumulation in n-3 PUFA-depleted diet-induced NAFLD model by altering microbiota composition and increasing production of GLP-1 [121]. Meanwhile, FOS supplementation stimulated fatty acid oxidation by activating peroxisome proliferatoractivated receptor-alpha (PPAR-α) and reduced cholesterol accumulation by inhibiting SREBP-2 in liver without affecting SREBP-1 expression and activity [121,122]. Lactulose is a prebiotic that promotes the growth of lactic acid bacteria and Bifidobacteria [123].…”

Section: Gut Microbiota-targeted Therapy With Prebioticmentioning

confidence: 99%

Gut Microbiota and Nonalcoholic Fatty Liver Disease: Insights on Mechanism and Therapy

Ma¹,

Zhou²,

Li³

2017

Preprint

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Gut microbiota play critical roles in development of obese-related metabolic diseases such as nonalcoholic fatty liver disease (NAFLD), type 2 diabetes, and insulin resistance, which highlighted the potential of gut microbiota-targeted therapies on these diseases. There are various ways that can manipulate gut microbiota including probiotics, prebiotics, synbiotics, antibiotics and some active components from herbal medicines. In this review, we first described the main roles of gut microbiota in mediating the development of NAFLD, and the advances in gut microbiota-targeted therapies in NAFLD in both the experimental and clinical studies, as well as the conclusions on the prospect of gut microbiotatargeted therapies in the future.

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Gut Microbiota: Association with NAFLD and Metabolic Disturbances

Cited by 74 publications

References 52 publications

Protective effect of quercetin on high-fat diet-induced non-alcoholic fatty liver disease in mice is mediated by modulating intestinal microbiota imbalance and related gut-liver axis activation

Protective effect of quercetin on high-fat diet-induced non-alcoholic fatty liver disease in mice is mediated by modulating intestinal microbiota imbalance and related gut-liver axis activation

Gut microbiota are linked to increased susceptibility to hepatic steatosis in low-aerobic-capacity rats fed an acute high-fat diet

Gut Microbiota and Nonalcoholic Fatty Liver Disease: Insights on Mechanism and Therapy

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