Olov Andersson

Olov Andersson

Principal Researcher | Docent
Telephone: +46852482927
Visiting address: Solnavägen 9, 17165 Stockholm
Postal address: C5 Cell- och molekylärbiologi, C5 CMB Andersson Olov, 171 77 Stockholm

About me

  • Interest:
    Bridging developmental biology, genetics and drug discovery, by using the zebrafish model to elucidate organogenesis and related mechanisms of disease.

    Positions:
    Principal Investigator 2012-present, Karolinska Institutet
    Postdoc 2008-2012, UCSF
    PhD 2002-2007, Karolinska Institutet
    Msc, Uppsala University

    Active grants:
    ERC Consolidator
    Novo Nordisk Foundation
    The Swedish Research Council
    Karolinska Institutet Consolidator
    Diabetesfonden
    Diabetes Wellness
    The Swedish Cancer Foundation
    SRP Diabetes, Karolinska Institutet
    Karolinska Institutet Doctoral student

    Awards:
    • Leif C. Groop award for outstanding diabetes research
    • ERC Consolidator Award
    • Novo Nordisk Foundation Excellence Project
    • Ragnar Söderberg Fellow in Medicine, from the Ragnar Söderberg’s Foundation
    • Ingvar Carlsson Award, from the Swedish Foundation of Strategic Research
    • Wenner-Gren Fellow appointed by the Wenner-Gren Foundation
    • EMBO, long-term postdoctoral fellowship
    • EMBO, short-term postdoctoral fellowship

Research

  • We are currently focusing on pancreatic beta-cell regeneration. Increasing the number of functional beta-cells might prove a better treatment for diabetes, which is at present controlled but not cured by insulin injections. Diabetes is characterized by elevated blood glucose levels, a consequence of insufficient insulin supply and/or insulin resistance. Despite mechanistic differences, both type 1 and late-stage type 2 diabetes feature a reduction in functional beta-cells. Experimental ablation of beta-cells by chemical treatment or partial pancreatectomy in zebrafish and rodents is followed by significant recovery of the beta-cell mass, indicating that the pancreas has the capacity to regenerate. This regenerative capacity could potentially be exploited therapeutically - if the underlying mechanisms were better understood.

    We perform unbiased chemical/genetic screens in zebrafish to identify compounds, genes and cellular mechanisms that promote beta-cell regeneration. The zebrafish model is particularly good for studying pancreatic development in vivo. First, the simplicity of its organ structures (e.g. the zebrafish embryo has only one pancreatic islet during the first week of development) allows rapid analysis of cellular changes. Second, zebrafish embryos are amenable to efficient transgenesis and drug delivery.

    By using a wide range of techniques, we are investigating several different cellular mechanisms of beta-cell regeneration:
    * Induction of beta-cell neogenesis
    * Promotion of beta-cell proliferation
    * Stimulation of beta-cell redifferentiation/maturation
    * Generation of ectopic insulin-producing cells

    In sum, we aim to identify and characterize compounds, signalling pathways and cellular mechanisms that can induce or increase beta-cell regeneration, with the overarching goal of developing new therapies for diabetes.

Articles

All other publications

Employments

  • Principal Researcher, Department of Cell and Molecular Biology, Karolinska Institutet, 2022-

Degrees and Education

  • Docent, Karolinska Institutet, 2019
  • Doctor Of Philosophy, Department of neuroscience, Karolinska Institutet, 2006

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