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PRIISM-HD SIGNED

Pathways Regulating Intramyocellular Insulin Sensitivity and Metabolism in Health and Disease

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 PRIISM-HD project word cloud

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

chemists    patients    mechanisms    ir    regulating    unifying    biologists    stuart    complementary    pharmacologists    actions    resistant    supervisor    pharmacological    pathogenesis    syndrome    employs    dysregulated    insulin    lipidomic    regulate    carolyn    skeletal    vivo    profiling    cummins    outgoing    glucose    strategy    nicely    significantly    driving    manipulation    integrating    understand    therapeutic    university    vitro    metabolism    dramatically    morgan    uncover    exemplified    homeostasis    genetic    dovetail    t2dm    mediating    proteomic    integrative    collaborative    network    gc    characterisations    locally    underpinning    metabolic    generation    dr    prevalence    normal    sk    toronto    sensitivity    disciplinary    expertise    lipid    potent    analytical    impacts    unclear    currently    muscle    resistance    intramyocellular    molecular    precise    urgent    researcher    glucocorticoids    diabetes    excess    phenotype    modulators    physiology    gcs    cushing   

Project "PRIISM-HD" data sheet

The following table provides information about the project.

Coordinator
THE UNIVERSITY OF BIRMINGHAM 

Organization address
address: Edgbaston
city: BIRMINGHAM
postcode: B15 2TT
website: www.bham.ac.uk

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
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 Coordinator Country United Kingdom [UK]
 Project website https://www.birmingham.ac.uk/staff/profiles/metabolism-systems/Morgan-Stuart.aspx
 Total cost 255˙349 €
 EC max contribution 255˙349 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2014
 Funding Scheme MSCA-IF-GF
 Starting year 2016
 Duration (year-month-day) from 2016-04-01   to  2020-11-11

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE UNIVERSITY OF BIRMINGHAM UK (BIRMINGHAM) coordinator 255˙349.00
2    THE GOVERNING COUNCIL OF THE UNIVERSITY OF TORONTO CA (TORONTO) partner 0.00

Map

 Project objective

Currently, there is an urgent need to understand the pathogenesis underpinning insulin resistance (IR) and type 2 diabetes (T2DM), due to their dramatically increasing prevalence. Glucocorticoids (GCs) are potent modulators of skeletal (Sk) muscle insulin sensitivity, as exemplified in patients with GC excess, Cushing’s syndrome, who develop IR and T2DM. Importantly, increased GC generation locally in muscle may contribute to the phenotype in T2DM patients. Although the precise molecular mechanisms driving IR in both T2DM and Cushing’s syndrome are unclear, dysregulated lipid metabolism is a common feature of insulin resistant muscle. This proposal aims to identify how GCs regulate intramyocellular lipid metabolism, and how this impacts on muscle insulin sensitivity. In addition, we will test a novel therapeutic target involved in mediating the metabolic actions of GCs, recently described by Dr Carolyn Cummins, the supervisor of the outgoing phase of this proposal. The complementary expertise in integrative molecular physiology of Dr Cummins, and of the Experienced Researcher, Dr Stuart Morgan, dovetail nicely within an established multi-disciplinary collaborative network of pharmacologists, molecular biologists and analytical chemists at the University of Toronto that have a unifying goal to uncover novel mechanisms regulating IR. Specifically, this proposal employs a systems approach by integrating both in vivo and in vitro pharmacological and genetic manipulation, with lipidomic/proteomic profiling and in-depth molecular characterisations. This novel strategy will significantly advance our understanding of key processes regulating insulin sensitivity in Sk muscle, a process essential for normal glucose homeostasis.

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