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Gould Lab @ Strathclyde

Regulation of Glucose Transport

Our work focusses upon mechanisms of membrane trafficking in health and disease, with emphasis on the control of glucose transporters and how this is disturbed in diabetes and cardiovascular disease.

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Gould Lab @ Strathclyde

A major consequence of insulin action is a dramatic increase in the rate of glucose transport into fat and muscle. This is achieved by the delivery of the facilitative glucose transporter GLUT4 from insulin-sensitive intracellular stores to the cell surface. Insulin-stimulated glucose transport is impaired in Type-2 diabetes; this is underpinned by reduced delivery of GLUT4 to the cell surface. Metabolic disorders such as Type-2 diabetes are linked to the development of cardiovascular disease. Cardiovascular disease represents the single biggest cause of death in T2DM and is independent of concurrent vascular disease.


Studies in our group seek to understand the cellular and molecular mechanisms which regulate glucose transport in adipocytes, cardiomyocytes and skeletal muscle. We focus upon the molecular machinery that control GLUT4 function, its interaction with the insulin signalling system, and defining how these systems are impaired in disease.


Our lab uses a range of experimental systems and approaches. These include studies of cultured adipocytes and genome-edited adipocytes, and iPSC-derived cardiomyocytes as our work-horse models, and employ approaches including imaging techniques such as confocal microscopy and dSTORM, analysis of signalling and trafficking in subcellular fractions and analysis of transport kinetics in intact cells. We also employ Saccharomyces cerevisiae as a tool to study membrane trafficking.

Projects

Projects are available in many areas, including those shown below.

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Dynamics of proteins in the plasma membrane

We are using advanced microscopy to study the dynamics of membrane protein behaviour at the surface of physiologically relevant cell types. We have identified complex behaviours of some proteins that we believe underlie their function and our work is resolving the molecular basis of how this behaviour is regulated.

Controlling SNARE complex formation

SNARE proteins are involved in all membrane trafficking events in mammalian cells. Specific interactions between SNARE proteins on the target membrane (t-SNAREs) with cognate SNAREs on the vesicle membrane (v-SNAREs) provides the minimal machinery required for membrane fusion. Regulation of SNARE complex function is a key control mechanism in membrane trafficking events.
Diabetes UK-funded work in our lab studies how insulin regualtes SNARE complex formation.

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Trafficking pathways for GLUT4

Insulin stimulates glucose transport in fat and muscle cells by triggering regulated delivery of intracellular vesicles containing the GLUT4 glucose transporter to the plasma membrane. This process is defective in diseases such as Type-2 Diabetes, underscoring the need to define trafficking pathways of GLUT4 and the molecular mechanisms that regulate them. Our work seeks to understand how GLUT4 trafficking is controlled in health and disease.

Adipokines: mechanism of release and functional characterisation

Fat cells secrete an array of adipokines - these have effects on other cells and tissues. Our work studies how these adipokines are released, how this is regulated and what the adipokines do.

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Role of Exosomes in insulin resistance

Factors circulating in the serum of patients with diabetes can cause cells to become 'insulin resistant'. We are studying the role of exosomes and adipocytokines in this phenomenon.

Outdoor Study Group

Publications

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Building GLUT4 vesicles.

A new review written with Frances Brodksy (UCL) and Nia Bryant (University of York)

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Insulin-stimulated GLUT4 translocation: size is not everything!

This review discusses whether the magnitude of GLUT4 translocation is all its cracked up to be!

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CHC22 clathrin mediates traffic from early secretory compartments for human GLUT4 pathway biogenesis.

A new route on the GLUT4 SatNav!

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Characterisation of GLUT4 trafficking in

HeLa cells.

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Here we discuss why HeLa cells, which do not normally express GLUT4, are a good model to study the trafficking of glucose transporters.

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Peter's graduate work examined how iPSC-derived cardiomyocytes transport glucose.

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Which vSNARE is most important for GLUT4 translocation? Jessica asked the question...

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GLUT4 dispersal in the adipocyte plasma membrane

Here Anna and Kamilla show that insulin-stimulated GLUT4 dispersal in the plasma membrane involves a novel protein complex.

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GLUT4 dispersal occurs in multiple cell types

Anna and Angéline show that GLUT4 dispersal operations in many cell types and may be defective in insulin resistance.

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Pleiotropic effects of Syntaxin16 identified by gene editing in cultured adipocytes

Shaun used CRISPR to delete adipocyte Syntaxin-16. Here is what he found.

Outdoor Study Group

Shannan Foylan

BBSRC-funded postdoc

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Angéline Geiser

EPSRC-funded PhD student

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Group Leader

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Justin Greig

PhD student funded by Medical Research Scotland

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Technician and Lab Guru

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EPSRC postdoc
[joint with Sebastian van de Linde]

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Get in Touch

Strathclyde Institute of Pharmacy and Biomedical Sciences,
University of Strathclyde,
161 Cathedral Street, Glasgow G4 0RE

44-141-548-4805

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SIPBS building at Strathclyde University
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