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Marjan Slak Rupnik
Prof. Dr. Marjan Slak Rupnik

Center for Physiology and Pharmacology (Institute of Physiology)
Position: Research Associate (Postdoc)

ORCID: 0000-0002-3744-4882
T +43 1 0664 5105888


Endocrinology; Insulin-Secreting Cells; Neuroendocrinology; Pancreas; Physiology

Research group(s)

Research interests

Our laboratory pioneered in pancreas tissue slices approach to study the function of insulin-secreting beta cells in adult (Speier and Rupnik, 2003; Rupnik 2009), perinatal mice (Meneghel-Rozzo et al., 2004; Rozzo et al., 2009), normal and diabetic rats (Rose at al., 2007),  as well as to establish the function of insulin-producing stem cells (Blyszczuk et al., 2005). We made significant contribution to  understanding of the function of KATP channels (Speier et al., 2005; Tsiaze et al, 2012), Munc18 (Mandic et al., 2011), NMDA receptors (Marquard et al., 2015), and SNAP25b (Daraio et al., 2017) within an intact pancreatic tissue. In addition we showed the crutial role and developmental aspect of cell-to-cell communication through Cx36 gap junctions in the activation, coordinated action and deactivation of beta cells (Rozzo et al, 2009; Speier et al., 2007; Rupnik 2009, Stozer and Rupnik, 2013).  The complex structure of the pancreatic islet network enabled us to describe emergent properties of the beta cell function in intact tissues (Stozer et al, 2013; Stozer et al, 2013, Dolenšek et al., 2013, Markovic et al., 2015, Gosak et al., 2015a,  Gosak et al., 2015b, Gosak et al., 2017a, Gosak et al., 2017b, Korosak and Slak Rupnik, 2018), 

Techniques, methods & infrastructure

  • patch-clamp & CCD imaging in fresh pancreas slices
  • confocal and multiphoton microscopy
  • computational cell collective analyses


  • R01DK127236 Control of beta cell function and survival by RYR2-mediated calcium signals (oo-ordinated by Carmella Evans-Molina, UI) (2021)
    Source of Funding: National Institutes of Health (NIH), Cellular Aspects of Diabetes and Obesity Study Section
    Principal Investigator
  • Beta-cells in diet-induced diabetes and remission (2019)
    Source of Funding: FWF (Austrian Science Fund), Joint Project; FWF-ARRS
    Coordinator of the collaborative project
  • Cell and Tissue Networks (2019)
    Source of Funding: Slovenian Research Agency (ARRS), Research Programs
    Principal Investigator
  • Linking Islet Cell Function and Identity from in vitro to in situ (2018)
    Source of Funding: National Institutes of Health (NIH), NIDKK - Human Islet Research Network
    Principal Investigator
  • pH-sensitive TALK1 channels in islet-ductal interactions (2017)
    Source of Funding: FWF (Austrian Science Fund), International Joint Project; FWF-MOST (Taiwan)
    Coordinator of the collaborative project
  • The role of TRPM3 and TRPM5 in the regulation of network activity in pancreatic islets (2017)
    Source of Funding: Slovenian Research Agency (ARRS), International Joint Project, FWO-ARRS
    Principal Investigator

Selected publications

  1. Sluga, N. et al. (2022) ‘Physiological levels of adrenaline fail to stop pancreatic beta cell activity at unphysiologically high glucose levels’, Frontiers in Endocrinology, 13. Available at:
  2. Korošak, D. et al. (2021) ‘Autopoietic Influence Hierarchies in Pancreatic, Cells’, Physical Review Letters, 127(16). Available at:
  3. Stožer, A. et al. (2021) ‘Glucose-dependent activation, activity, and deactivation of beta cell networks in acute mouse pancreas tissue slices’, American Journal of Physiology-Endocrinology and Metabolism, 321(2), pp. E305–E323. Available at:
  4. Korošak, D. and Slak Rupnik, M. (2018) ‘Collective Sensing of β-Cells Generates the Metabolic Code’, Frontiers in Physiology, 9. Available at:
  5. Marquard, J. et al. (2015) ‘Characterization of pancreatic NMDA receptors as possible drug targets for diabetes treatment’, Nature Medicine, 21(4), pp. 363–372. Available at: