Exposure to nitenpyram during pregnancy causes colonic mucosal damage and non-alcoholic steatohepatitis in mouse offspring: The role of gut microbiota

Herein, we investigate whether: (1) the administration of glucose or a lipid emulsion is useful in liver transplantation (LT) using steatotic (induced genetically or nutritionally) or non-steatotic livers from donors after brain death (DBDs); and (2) any such benefits are due to reductions in intestinal damage and consequently to gut microbiota preservation. In recipients from DBDs, we show increased hepatic damage and failure in the maintenance of ATP, glycogen, phospholipid and growth factor (HGF, IGF1 and VEGFA) levels, compared to recipients from non-DBDs. In recipients of non-steatotic grafts from DBDs, the administration of glucose or lipids did not protect against hepatic damage. This was associated with unchanged ATP, glycogen, phospholipid and growth factor levels. However, the administration of lipids in steatotic grafts from DBDs protected against damage and ATP and glycogen drop and increased phospholipid levels. This was associated with increases in growth factors. In all recipients from DBDs, intestinal inflammation and damage (evaluated by LPS, vascular permeability, mucosal damage, TLR4, TNF, IL1, IL-10, MPO, MDA and edema formation) was not shown. In such cases, potential changes in gut microbiota would not be relevant since neither inflammation nor damage was evidenced in the intestine following LT in any of the groups evaluated. In conclusion, lipid treatment is the preferable nutritional support to protect against hepatic damage in steatotic LT from DBDs; the benefits were independent of alterations in the recipient intestine.

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Gut microbiota modulation as a promising therapy with metformin in rats with non-alcoholic steatohepatitis: Role of LPS/TLR4 and autophagy pathways

European Journal of Pharmacology ◽

10.1016/j.ejphar.2020.173461 ◽

2020 ◽

Vol 887 ◽

pp. 173461

Author(s):

Lamiaa A. Ahmed ◽

Maha B. Salem ◽

Sayed H. Seif el-Din ◽

Naglaa M. El-Lakkany ◽

Hend O. Ahmed ◽

...

Keyword(s):

Gut Microbiota ◽

Alcoholic Steatohepatitis

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Flaxseed Powder Attenuates Non-Alcoholic Steatohepatitis via Modulation of Gut Microbiota and Bile Acid Metabolism through Gut–Liver Axis

International Journal of Molecular Sciences ◽

10.3390/ijms221910858 ◽

2021 ◽

Vol 22 (19) ◽

pp. 10858

Author(s):

Chao Yang ◽

Min Wan ◽

Dengfeng Xu ◽

Da Pan ◽

Hui Xia ◽

...

Keyword(s):

Bile Acid ◽

Gut Microbiota ◽

Normal Diet ◽

Bile Acid Metabolism ◽

Alcoholic Fatty Liver ◽

Beneficial Effects ◽

Alcoholic Steatohepatitis ◽

And Control ◽

Different Doses

Non-alcoholic steatohepatitis (NASH) is gradually becoming one of the most common and health-endangering diseases; therefore, it is very important to prevent the occurrence of NASH and prevent simple non-alcoholic fatty liver (NAFL) from further developing into NASH. We fed mice a high-fat diet (HFD, 60% fat) for 14 weeks to induce NAFL and then fed different doses of flaxseed powder (low (10%), middle (20%), and high (30%)) to the mice for 28 weeks. After the animal experiment, we analyzed fecal bile acid (BA) profiles of the HFD mice, flaxseed-fed (FLA-fed) mice, and control mice with a normal diet (10% fat) using a targeted metabolomics approach, and we analyzed the gut microbiota at the same time. We also investigated the mechanistic role of BAs in NASH and identified whether the altered BAs strongly bind to colonic FXR or TGR5. In the present study, we found that 28-week FLA treatment notably alleviated NASH development in NAFL model mice fed with an HFD, and the beneficial effects may be attributed to the regulation of and improvement in the gut flora- and microbiota-related BAs, which then activate the intestinal FXR-FGF15 and TGR5-NF-κB pathways. Our data indicate that FLA might be a promising functional food for preventing NASH through regulating microbiomes and BAs.

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Dual role of B7 costimulation in obesity-related non-alcoholic steatohepatitis (NASH) and metabolic dysregulation

Experimental and Clinical Endocrinology & Diabetes ◽

10.1055/s-0034-1372182 ◽

2014 ◽

Vol 122 (03) ◽

Author(s):

A Chatzigeorgiou ◽

R Garcia-Martin ◽

KJ Chung ◽

I Alexaki ◽

A Klotzsche-von Ameln ◽

...

Keyword(s):

Dual Role ◽

Alcoholic Steatohepatitis ◽

Metabolic Dysregulation

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Gut Microbiota and Antipsychotics Induced Metabolic Alteration

Global Clinical and Translational Research ◽

10.36316/gcatr.01.0020 ◽

2019 ◽

pp. 131-143

Author(s):

Dong-Yu Kan ◽

Su-Juan Li ◽

Chen-Chen Liu ◽

Ren-Rong Wu

Keyword(s):

Gut Microbiota ◽

Body Weight Gain ◽

Neuropsychiatric Disorders ◽

Elevated Risk ◽

Metabolic Disturbance ◽

Metabolic Dysfunction ◽

Sequencing Technology ◽

Severe Mental Disorder ◽

Metabolic Alteration

Schizophrenia is a chronic and severe mental disorder with antipsychotics as primary medications, but the antipsychotic-induced metabolic side effects may contribute to the elevated risk of overall morbidity and mortality in patients with psych-iatric diseases. With the development in sequencing technology and bioinformatics, dysbiosis has been shown to contribute to body weight gain and metabolic dysfunction. However, the role of gut microbiota in the antipsychotic-induced metabolic alteration remains unknown. In this paper, we reviewed the recent studies of the gut microbiota with psychiatric disorders and antipsychotic-induced metabolic dysfunction. Patients with neuropsychiatric disorders may have a different composi-tion of gut microbiota compared with healthy controls. In addition, it seems that the use of antipsychotics is concurrently associated with both altered composition of gut microbiota and metabolic disturbance. Further study is needed to address the role of gut microbiota in the development of neuropsychiatric disorders and antipsychotic-induced metabolic disturbance, to develop novel therapeutics for both neuropsychiatric disorders and metabolic dysfunction.

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The possible protective role of pumpkin seed oil in ameliorating tongue mucosal damage induced by orlistat in adult male albino rats: A light and scanning electron microscopic study

Egyptian Journal of Histology ◽

10.21608/ejh.2020.25027.1258 ◽

2020 ◽

Vol 0 (0) ◽

pp. 0-0

Author(s):

Amira Kassab ◽

Khalid Ahmed Moustafa ◽

Amal Abd-El-Hafez

Keyword(s):

Seed Oil ◽

Mucosal Damage ◽

Protective Role ◽

Albino Rats ◽

Electron Microscopic ◽

Pumpkin Seed ◽

Scanning Electron Microscopic Study ◽

Scanning Electron Microscopic ◽

Pumpkin Seed Oil

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Multiple Sclerosis, Gut Microbiota and Permeability: Role of Tryptophan Catabolites, Depression and the Driving Down of Local Melatonin

Current Pharmaceutical Design ◽

10.2174/1381612822666160915160520 ◽

2016 ◽

Vol 22 (40) ◽

pp. 6134-6141 ◽

Cited By ~ 15

Author(s):

Moses Rodriguez ◽

Bharath Wootla ◽

George Anderson

Keyword(s):

Multiple Sclerosis ◽

Gut Microbiota ◽

Tryptophan Catabolites

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Microbiota-Immune System Interactions in Human Neurological Disorders

CNS & Neurological Disorders - Drug Targets ◽

10.2174/1871527319666200726222138 ◽

2020 ◽

Vol 19 (7) ◽

pp. 509-526

Author(s):

Qin Huang ◽

Fang Yu ◽

Di Liao ◽

Jian Xia

Keyword(s):

Immune System ◽

Gut Microbiota ◽

Neurological Disorders ◽

Brain Function ◽

Neurological Diseases ◽

Host Immune System ◽

Gut Dysbiosis ◽

Characteristic Features ◽

Novel Therapeutic Strategies

: Recent studies implicate microbiota-brain communication as an essential factor for physiology and pathophysiology in brain function and neurodevelopment. One of the pivotal mechanisms about gut to brain communication is through the regulation and interaction of gut microbiota on the host immune system. In this review, we will discuss the role of microbiota-immune systeminteractions in human neurological disorders. The characteristic features in the development of neurological diseases include gut dysbiosis, the disturbed intestinal/Blood-Brain Barrier (BBB) permeability, the activated inflammatory response, and the changed microbial metabolites. Neurological disorders contribute to gut dysbiosis and some relevant metabolites in a top-down way. In turn, the activated immune system induced by the change of gut microbiota may deteriorate the development of neurological diseases through the disturbed gut/BBB barrier in a down-top way. Understanding the characterization and identification of microbiome-immune- brain signaling pathways will help us to yield novel therapeutic strategies by targeting the gut microbiome in neurological disease.

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10 THE ROLE OF DIETARY L-SERINE IN THE REGULATION OF INTESTINAL MUCUS BARRIER DURING INFLAMMATION

Inflammatory Bowel Diseases ◽

10.1093/ibd/zaa010.110 ◽

2020 ◽

Vol 26 (Supplement_1) ◽

pp. S42-S42

Author(s):

Kohei Sugihara ◽

Nobuhiko Kamada

Keyword(s):

Amino Acids ◽

Amino Acid ◽

Gut Microbiota ◽

Control Diet ◽

Bacterial Strains ◽

Germ Free ◽

Intestinal Mucus ◽

Gnotobiotic Mice ◽

Mucus Barrier

Abstract Background Recent accumulating evidence suggests that amino acids have crucial roles in the maintenance of intestinal homeostasis. In inflammatory bowel disease (IBD), amino acid metabolism is changed in both host and the gut microbiota. Among amino acids, L-serine plays a central role in several metabolic processes that are essential for the growth and survival of both mammalian and bacterial cells. However, the role of L-serine in intestinal homeostasis and IBD remains incompletely understood. In this study, we investigated the effect of dietary L-serine on intestinal inflammation in a murine model of colitis. Methods Specific pathogen-free (SPF) mice were fed either a control diet (amino acid-based diet) or an L-serine-deficient diet (SDD). Colitis was induced by the treatment of dextran sodium sulfate (DSS). The gut microbiome was analyzed by 16S rRNA sequencing. We also evaluate the effect of dietary L-serine in germ-free mice and gnotobiotic mice that were colonized by a consortium of non-mucolytic bacterial strains or the consortium plus mucolytic bacterial strains. Results We found that the SDD exacerbated experimental colitis in SPF mice. However, the severity of colitis in SDD-fed mice was comparable to control diet-fed mice in germ-free condition, suggesting that the gut microbiota is required for exacerbation of colitis caused by the restriction of dietary L-serine. The gut microbiome analysis revealed that dietary L-serine restriction fosters the blooms of a mucus-degrading bacterium Akkermansia muciniphila and adherent-invasive Escherichia coli in the inflamed gut. Consistent with the expansion of mucolytic bacteria, SDD-fed mice showed a loss of the intestinal mucus layer. Dysfunction of the mucus barrier resulted in increased intestinal permeability, thereby leading to bacterial translocation to the intestinal mucosa, which subsequently increased the severity of colitis. The increased intestinal permeability and subsequent bacterial translocation were observed in SDD-fed gnotobiotic mice that colonized by mucolytic bacteria. In contrast, dietary L-serine restriction did not alter intestinal barrier integrity in gnotobiotic mice that colonized only by non-mucolytic bacteria. Conclusion Our results suggest that dietary L-serine regulates the integrity of the intestinal mucus barrier during inflammation by limiting the expansion of mucus degrading bacteria.

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