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  1. Article ; Online: Gut microbiota modulation with norfloxacin and ampicillin enhances glucose tolerance in mice.

    Membrez, Mathieu / Blancher, Florence / Jaquet, Muriel / Bibiloni, Rodrigo / Cani, Patrice D / Burcelin, Rémy G / Corthesy, Irène / Macé, Katherine / Chou, Chieh Jason

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2008  Volume 22, Issue 7, Page(s) 2416–2426

    Abstract: Recent data suggest that the gut microbiota plays a significant role in fat accumulation. However, it is not clear whether gut microbiota is involved in the pathophysiology of type 2 diabetes. To assess this issue, we modulated gut microbiota via ... ...

    Abstract Recent data suggest that the gut microbiota plays a significant role in fat accumulation. However, it is not clear whether gut microbiota is involved in the pathophysiology of type 2 diabetes. To assess this issue, we modulated gut microbiota via antibiotics administration in two different mouse models with insulin resistance. Results from dose-determination studies showed that a combination of norfloxacin and ampicillin, at a dose of 1 g/L, maximally suppressed the numbers of cecal aerobic and anaerobic bacteria in ob/ob mice. After a 2-wk intervention with the antibiotic combination, both ob/ob and diet-induced obese and insulin-resistant mice showed a significant improvement in fasting glycemia and oral glucose tolerance. The improved glycemic control was independent of food intake or adiposity because pair-fed ob/ob mice were as glucose intolerant as the control ob/ob mice. Reduced liver triglycerides and increased liver glycogen correlated with improved glucose tolerance in the treated mice. Concomitant reduction of plasma lipopolysaccharides and increase of adiponectin further supported the antidiabetic effects of the antibiotic treatment in ob/ob mice. In summary, modulation of gut microbiota ameliorated glucose tolerance of mice by altering the expression of hepatic and intestinal genes involved in inflammation and metabolism, and by changing the hormonal, inflammatory, and metabolic status of the host.
    MeSH term(s) Ampicillin/pharmacology ; Animals ; Anti-Bacterial Agents/pharmacology ; Bacteroides/drug effects ; Bacteroides/physiology ; Bifidobacterium/drug effects ; Bifidobacterium/physiology ; Diabetes Mellitus, Type 2/etiology ; Diabetes Mellitus, Type 2/physiopathology ; Enterobacteriaceae/drug effects ; Enterobacteriaceae/physiology ; Lactobacillus/drug effects ; Lactobacillus/physiology ; Mice ; Mice, Obese ; Microbial Sensitivity Tests ; Norfloxacin/pharmacology ; Obesity/microbiology ; Obesity/physiopathology
    Chemical Substances Anti-Bacterial Agents ; Ampicillin (7C782967RD) ; Norfloxacin (N0F8P22L1P)
    Language English
    Publishing date 2008-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.07-102723
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2266: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 296: Show issues

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  2. Article: Gut microbiota modulation with norfloxacin and ampicillin enhances glucose tolerance in mice

    Membrez, Mathieu / Blancher, Florence / Jaquet, Muriel / Bibiloni, Rodrigo / Cani, Patrice D / Burcelin, Rémy G / Corthesy, Irène / Macé, Katherine / Chou, Chieh Jason

    FASEB journal. 2008 July, v. 22, no. 7

    2008  

    Abstract: Recent data suggest that the gut microbiota plays a significant role in fat accumulation. However, it is not clear whether gut microbiota is involved in the pathophysiology of type 2 diabetes. To assess this issue, we modulated gut microbiota via ... ...

    Abstract Recent data suggest that the gut microbiota plays a significant role in fat accumulation. However, it is not clear whether gut microbiota is involved in the pathophysiology of type 2 diabetes. To assess this issue, we modulated gut microbiota via antibiotics administration in two different mouse models with insulin resistance. Results from dose-determination studies showed that a combination of norfloxacin and ampicillin, at a dose of 1g/L, maximally suppressed the numbers of cecal aerobic and anaerobic bacteria in ob/ob mice. After a 2-wk intervention with the antibiotic combination, both ob/ob and diet-induced obese and insulin-resistant mice showed a significant improvement in fasting glycemia and oral glucose tolerance. The improved glycemic control was independent of food intake or adiposity because pair-fed ob/ob mice were as glucose intolerant as the control ob/ob mice. Reduced liver triglycerides and increased liver glycogen correlated with improved glucose tolerance in the treated mice. Concomitant reduction of plasma lipopolysaccharides and increase of adiponectin further supported the antidiabetic effects of the antibiotic treatment in ob/ob mice. In summary, modulation of gut microbiota ameliorated glucose tolerance of mice by altering the expression of hepatic and intestinal genes involved in inflammation and metabolism, and by changing the hormonal, inflammatory, and metabolic status of the host.--Membrez, M., Blancher, F., Jaquet, M., Bibiloni, R., Cani, P. D., Burcelin, R. G., Corthesy, I., Macé, K., Chou, C. J. Gut microbiota modulation with norfloxacin and ampicillin enhances glucose tolerance in mice.
    Language English
    Dates of publication 2008-07
    Size p. 2416-2426.
    Publishing place The Federation of American Societies for Experimental Biology
    Document type Article
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    Database NAL-Catalogue (AGRICOLA)

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  3. Article: Bacterial colitis increases susceptibility to oral prion disease.

    Sigurdson, Christina J / Heikenwalder, Mathias / Manco, Giuseppe / Barthel, Manja / Schwarz, Petra / Stecher, Bärbel / Krautler, Nike J / Hardt, Wolf-Dietrich / Seifert, Burkhardt / MacPherson, Andrew J S / Corthesy, Irène / Aguzzi, Adriano

    The Journal of infectious diseases

    2006  Volume 199, Issue 2, Page(s) 243–252

    Abstract: Dietary exposure to prion-contaminated materials has caused kuru and variant Creutzfeldt-Jakob disease in humans and transmissible spongiform encephalopathies (TSEs) in cattle, mink, and felines. The epidemiology of dietary prion infections suggests that ...

    Abstract Dietary exposure to prion-contaminated materials has caused kuru and variant Creutzfeldt-Jakob disease in humans and transmissible spongiform encephalopathies (TSEs) in cattle, mink, and felines. The epidemiology of dietary prion infections suggests that host genetic modifiers and possibly exogenous cofactors may play a decisive role in determining disease susceptibility. However, few cofactors influencing susceptibility to prion infection have been identified. In the present study, we investigated whether colitis might represent one such cofactor. We report that moderate colitis caused by an attenuated Salmonella strain more than doubles the susceptibility of mice to oral prion infection and modestly accelerates the development of disease after prion challenge. The prion protein was up-regulated in intestines and mesenteric lymph nodes of mice with colitis, providing a possible mechanism for the effect of colitis on the pathogenesis of prion disease. Therefore, moderate intestinal inflammation at the time of prion exposure may constitute one of the elusive risk factors underlying the development of TSE.
    MeSH term(s) Animals ; Cecum/metabolism ; Disease Susceptibility ; Enterocolitis/complications ; Enterocolitis/microbiology ; Mice ; Mice, Inbred C57BL ; Mouth Diseases/complications ; Mouth Diseases/metabolism ; PrPC Proteins/metabolism ; PrPSc Proteins/metabolism ; Prion Diseases/complications ; Prion Diseases/metabolism ; Prions/metabolism ; Prions/pathogenicity ; Risk Factors ; Salmonella Infections/complications ; Salmonella Infections/microbiology ; Salmonella typhimurium/genetics ; Salmonella typhimurium/pathogenicity ; Scrapie/complications ; Scrapie/metabolism ; Specific Pathogen-Free Organisms
    Chemical Substances PrPC Proteins ; PrPSc Proteins ; Prions
    Language English
    Publishing date 2006-12-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3019-3
    ISSN 1537-6613 ; 0022-1899
    ISSN (online) 1537-6613
    ISSN 0022-1899
    DOI 10.1086/595791
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uh II Zs.50: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
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    Zs.MO 445: Show issues

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