β-Cells at the crossroads: choosing between insulin granule production and proliferation

Authors

  • Yanmei Liu,

    1. Molecular Diabetology, Paul Langerhans Institute Dresden, School of Medicine and University Clinic ‘Carl Gustav Carus', Dresden University of Technology, Dresden 0130, Germany
    2. Max Planck Institute of Molecular Cell Biology and Genetics, Dresden 01307, Germany
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  • Hassan Mziaut,

    1. Molecular Diabetology, Paul Langerhans Institute Dresden, School of Medicine and University Clinic ‘Carl Gustav Carus', Dresden University of Technology, Dresden 0130, Germany
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  • Anna Ivanova,

    1. Molecular Diabetology, Paul Langerhans Institute Dresden, School of Medicine and University Clinic ‘Carl Gustav Carus', Dresden University of Technology, Dresden 0130, Germany
    2. Max Planck Institute of Molecular Cell Biology and Genetics, Dresden 01307, Germany
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  • Michele Solimena

    Corresponding author
    1. Molecular Diabetology, Paul Langerhans Institute Dresden, School of Medicine and University Clinic ‘Carl Gustav Carus', Dresden University of Technology, Dresden 0130, Germany
    2. Internal Medicine III, School of Medicine and University Clinic ‘Carl Gustav Carus', Dresden University of Technology, Dresden 01307, Germany
    3. Max Planck Institute of Molecular Cell Biology and Genetics, Dresden 01307, Germany
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Michele Solimena, Molecular Diabetology, Paul Langerhans Institute Dresden, School of Medicine and University Clinic ‘Carl Gustav Carus', Dresden University of Technology, Dresden 0130, Germany.
E-mail:
michele.solimena@tu-dresden.de

Abstract

Pancreatic β-cells are the sole source of insulin, the major hormonal regulator of glycaemia. In physiological and pathological conditions with increased insulin demand, β-cells adjust their insulin output either through increased insulin secretory granule (ISG) biogenesis and secretion, or hyperplasia. Failure of these compensatory mechanisms eventually results in hyperglycaemia and diabetes mellitus. Both of these major adaptive behaviours are positively regulated by several extrinsic factors, such as glucose, GLP-1, insulin and growth hormones (GH). Still unclear, however, it is how β-cells in response to these stimuli opt for one or the other strategy at a given time. Here we review recent advances concerning the factors and pathways that enhance ISG biogenesis and β-cell replication, and propose the existence of ‘switch factors' that play a key role in regulating the shift between these two adaptive responses.

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