Pyrroloquinoline Quinone-Secreting Probiotic<i>Escherichia coli</i>Nissle 1917 Ameliorates Ethanol-Induced Oxidative Damage and Hyperlipidemia in Rats

Singh, Ashish; Pandey, Sumeet; Archana, G.

doi:10.1111/acer.12456

Cited by 36 publications

(24 citation statements)

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“…Engineered PQQsecreting E. coli str. Nissle protected against hepatic hyperlipidaemia in a rat model of ethanolinduced liver damage 229 , supporting PQQ as a potential novel strategy to reduce risk of NAFLD development. The key to optimizing probiotic or prebiotic approaches are functional maps of both healthy and obese gut microbiota, particularly for infants, which are only just being investigated 230 .…”

Section: Targeting the Gut–liver Axismentioning

confidence: 84%

Developmental origins of NAFLD: a womb with a clue

Wesolowski

Kasmi

Jonscher

et al. 2016

Nat Rev Gastroenterol Hepatol

180

167

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Changes in the maternal environment leading to an altered intrauterine milieu can result in subtle insults to the fetus, promoting increased lifetime disease risk and/or disease acceleration in childhood and later in life. Particularly worrisome is that the prevalence of NAFLD is rapidly increasing among children and adults, and is being diagnosed at increasingly younger ages, pointing towards an early-life origin. A wealth of evidence, in humans and non-human primates, suggests that maternal nutrition affects the placenta and fetal tissues, leading to persistent changes in hepatic metabolism, mitochondrial function, the intestinal microbiota, liver macrophage activation and susceptibility to NASH postnatally. Deleterious exposures in utero include fetal hypoxia, increased nutrient supply, inflammation and altered gut microbiota that might produce metabolic clues, including fatty acids, metabolites, endotoxins, bile acids and cytokines, which prime the infant liver for NAFLD in a persistent manner and increase susceptibility to NASH. Mechanistic links to early disease pathways might involve shifts in lipid metabolism, mitochondrial dysfunction, pioneering gut microorganisms, macrophage programming and epigenetic changes that alter the liver microenvironment, favouring liver injury. In this Review, we discuss how maternal, fetal, neonatal and infant exposures provide developmental clues and mechanisms to help explain NAFLD acceleration and increased disease prevalence. Mechanisms identified in clinical and preclinical models suggest important opportunities for prevention and intervention that could slow down the growing epidemic of NAFLD in the next generation.NAFLD is a general term used to describe a broad spectrum of liver abnormalities, ranging from simple, uncomplicated hepatic steatosis to NASH, accompanied by different degrees of Correspondence to J.E.F. jed.friedman@ucdenver.edu. Author contributionsAll authors researched data for the article, provided a substantial contribution to discussion of content, wrote the article, and reviewed and edited the manuscript before submission. Competing interests statementThe authors declare no competing interests. HHS Public AccessAuthor manuscript Nat Rev Gastroenterol Hepatol. Author manuscript; available in PMC 2017 December 12. Author Manuscript Author ManuscriptAuthor ManuscriptAuthor Manuscript inflammation and fibrosis. NAFLD is increasing in prevalence, especially in adolescents 1 , despite the levellingoff of the obesity epidemic from 2003-2004 to 2013-2014 in children and adolescents aged 2-19 years (REF.2). The most common chronic liver disease worldwide, NAFLD increases the risk of cardiovascular events eightfold and type 2 diabetes mellitus (T2DM) threefold 3 , and is a strong risk factor for hepatocellular carcinoma (HCC) 4 . At the time of paediatric NAFLD diagnosis, 25-50% of children have NASH and 10-25% have advanced fibrosis 5 . For many decades, it was thought that NAFLD was predominantly driven by obesity in the setting of genetic suscep...

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Section: Targeting the Gut–liver Axismentioning

confidence: 84%

Developmental origins of NAFLD: a womb with a clue

Wesolowski

Kasmi

Jonscher

et al. 2016

Nat Rev Gastroenterol Hepatol

180

167

View full text Add to dashboard Cite

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“…With the development of modern intensive farming, chickens are prone to oxidative stress (Salami, Majoka, Saha, Garber, & Gabarrou, ). Numerous studies found that dietary probiotics in diets were beneficial in oxidation resistance, scavenging ROS and promoting antioxidant capability (Chen, Gong, & Xu, ; Singh, Pandey, & Naresh, ). Antioxidant enzymes (SOD, CAT, GSH and GSH‐Px) serve as the first line to suppress the oxidative damage.…”

Section: Discussionmentioning

confidence: 99%

Effects of Bacillus subtilis C‐3102 on production, hatching performance, egg quality, serum antioxidant capacity and immune response of laying breeders

Liu

Canyang

et al. 2018

Animal Physiology Nutrition

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To investigate the supplemental effects of Bacillus subtilis C‐3102 on the production, hatching performance, egg quality, serum antioxidant capacity and immune response of laying breeders, a total of 480 Xuefeng black‐bone (25‐week‐old) hens were randomly assigned into four treatment groups: Hens fed the basal diets with 0 (CON), 3.0 × 105 (BS‐1), 6.0 × 105 cfu/g (BS‐2) and 9.0 × 105 (BS‐3) cfu/g of B. subtilis C‐3102. As the B. subtilis C‐3102 level increased, egg weight (linear, p < 0.01; quadratic, p = 0.003), fertility (linear, p = 0.021; quadratic, p = 0.059), hatchability (linear, p = 0.038; quadratic, p = 0.119) and yolk colour (linear, p = 0.006; quadratic, p = 0.021) increased in a linear or quadratic manner. Yolk index increased quadratically (linear, p = 0.054; quadratic, p = 0.017), and eggshell thickness (linear, p = 0.036; quadratic, p = 0.128), the activity of GSH‐Px (linear, p = 0.024; quadratic, p = 0.078), the concentration of IgM (linear, p = 0.016; quadratic, p = 0.056) and the level of AIV‐Ab (linear, p = 0.034; quadratic, p = 0.103) in the serum increased linearly as dietary supplementation of B. subtilis C‐3102 increased. The results showed that dietary treatments did not affect egg production, feed conversion ratio, egg mass, hatchability of fertile eggs, eggshell‐breaking strength, egg‐shape index, yolk percentage, Haugh unit, T‐SOD, T‐AOC, MDA, IgA and IgG concentrations and the level of NDV‐Ab in the serum. In conclusion, dietary supplementation of 9.0 × 105 cfu/g B. subtilis C‐3102 in laying breeders diets may be a feasible means of effectively increasing egg weight, fertility and hatchability, and improving egg quality such as eggshell thickness, yolk index and yolk colour. Besides, B. subtilis C‐3102 can enhance the activity of GSH‐Px, the concentration of IgM and the level of AIV‐Ab in the serum.

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“…Evidences suggest that PQQ can permeate to subcellular organelles such as mitochondria (Stites et al, 2006). In the present study 3.7 kb pqqABCDE gene cluster from G. oxydans 621H was used to reduce the plasmid load in contrast to our earlier reports of 13.3 kb pqq gene cluster from Pseudomonas fluorescens B16 Singh et al, 2014).…”

Section: Discussionmentioning

confidence: 66%

“…PQQ was extracted from the bacterial strains as described by Suzuki et al (1990) and used by Singh et al (2014). Faeces and liver homogenate were collected for PQQ estimations from rat gut lumen and liver tissues, respectively.…”

Section: Pqq Extraction and Quantificationmentioning

confidence: 99%

“…EcN was genetically modified by incorporating PQQ producing operon and was used as a novel endogenous delivery system by exploiting the potential of probiotic Escherichia coli strains Singh et al, 2014). Consistent endogenous production and secretion of PQQ in the gut by EcN was shown to be effective in reducing oxidative stress, mitochondrial dysfunction and altered lipid profile in ras.…”

Section: Introductionmentioning

confidence: 99%

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