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BETA-BACT SIGNED

Beta-cell inflammation and dysfunction induced by bacterial translocation

Total Cost €

0

EC-Contrib. €

0

Partnership

0

Views

0

 BETA-BACT project word cloud

Explore the words cloud of the BETA-BACT project. It provides you a very rough idea of what is the project "BETA-BACT" about.

tlr    induce    progressive    epidemic    islets    diabetes    translocation    treatment    insulin    cultured    therapies    translocated    pancreatectomy    composition    exogenous    type    trl4    pancreatic    associate    demonstrated    direct    first    causes    leaky    unknown    intestinal    pancreas    central    reverse    mechanisms    dysfunction    previously    inflammation    bacteria    cells    harvested    course    glucose    warranted    inflammatory    t2d    aerobically    induces    destruction    toll    cell    effects    hypothesis    gut    hypothesized    tissue    bacterial    adipose    trigger    halt    detrimental    metabolism    microorganism    impaired    producing    receptors    langerhans    action    continuous    pathogenicity    function    shown    immune    model    resistance    load    pilot    obese    beta    subsequently    gavage    ing    dna    alterations    micro    microbiota    data    disease    infiltration    highest    knockout    patients    mouse    form    diet    morbidity    hyperglycemia    mortality    therapy    organisms    proportions    primary   

Project "BETA-BACT" data sheet

The following table provides information about the project.

Coordinator
STICHTING VUMC 

Organization address
address: DE BOELELAAN 1117
city: AMSTERDAM
postcode: 1081 HV
website: www.vumc.nl

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Netherlands [NL]
 Project website http://ec.europa.eu/research/mariecurieactions/about/individual-fellowships_en
 Total cost 167˙610 €
 EC max contribution 167˙610 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2015
 Funding Scheme MSCA-IF-GF
 Starting year 2016
 Duration (year-month-day) from 2016-06-01   to  2018-12-01

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    STICHTING VUMC NL (AMSTERDAM) coordinator 167˙610.00
2    STICHTING VU NL (AMSTERDAM) participant 0.00
3    UNIVERSITY OF BRITISH COLUMBIA CA (VANCOUVER) partner 0.00

Map

 Project objective

Type 2 diabetes (T2D) has risen to epidemic proportions resulting in major morbidity and mortality. In addition to insulin resistance (i.e. impaired insulin action), impaired function and destruction of the insulin-producing beta cells form the direct cause for hyperglycemia and T2D, and causes the progressive course of disease. As such, due to continuous beta-cell destruction, many patients require treatment with exogenous insulin therapy. Clearly, therapies that may halt or reverse this detrimental process are warranted. An inflammatory process in islets of Langerhans, with infiltration of immune cells and a central role for toll-like receptors (TLR), is present in T2D, however, the primary trigger for this inflammatory response remains unknown. Recently, (diet-induced) alterations in intestinal microbiota composition were shown to associate with T2D. In addition, T2D patients have increased translocation of detrimental bacteria (‘leaky gut’), previously shown to induce adipose tissue inflammation and dysfunction. Recently, I hypothesized that increased bacterial translocation to the pancreas induces inflammation and beta-cell dysfunction in T2D through TLR related mechanisms. I addressed this hypothesis first by identifying translocated microorganism DNA in pancreatic tissue harvested during pancreatectomy in patients with and without T2D. In pilot data, I have demonstrated increased bacterial load in patients with T2D as compared to control patients. The involved micro organisms with highest pathogenicity will be (an)aerobically cultured and subsequently used in gavage studies in a obese mouse model with or without a knockout for TRL4 to study their effects effects on beta-cell function, glucose metabolism and pancreas inflammation.

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The information about "BETA-BACT" are provided by the European Opendata Portal: CORDIS opendata.

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