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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. Our lab uses cellular and systems biology approaches to understand insulin-regulated GLUT4 trafficking in different cells.
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.
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Diabetes. Umwelt. Leben. Perspektiven aus allen Blickwinkeln Diabetologie und Stoffwechsel (2024)
BIOMOLECULESno. 12 (2023)
Bioscience reportsno. 10 (2023)
Endocrine Abstracts (2023)
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BRITISH JOURNAL OF PHARMACOLOGY (2023): 561-562
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BRITISH JOURNAL OF PHARMACOLOGY (2023): 669-670
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