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Hindrik Mulder

Hindrik Mulder

Principal investigator

Hindrik Mulder

Islet beta-cell area and hormone expression are unaltered in Huntington's disease.


  • Karl Bacos
  • Maria Björkqvist
  • Åsa Petersén
  • Lena Luts
  • Marion Maat-Schieman
  • Raymund Roos
  • Frank Sundler
  • Patrik Brundin
  • Hindrik Mulder
  • Nils Wierup

Summary, in English

Neurodegenerative disorders are often associated with metabolic alterations. This has received little attention, but might be clinically important because it can contribute to symptoms and influence the course of the disease. Patients with Huntington's disease (HD) exhibit increased incidence of diabetes mellitus (DM). This is replicated in mouse models of HD, e.g., the R6/2 mouse, in which DM is primarily caused by a deficiency of beta-cells with impaired insulin secretion. Pancreatic tissue from HD patients has previously not been studied and, thus, the pathogenesis of DM in HD is unclear. To address this issue, we examined pancreatic tissue sections from HD patients at different disease stages. We found that the pattern of insulin immunostaining, levels of insulin transcripts and islet beta-cell area were similar in HD patients and controls. Further, there was no sign of amyloid deposition in islets from HD patients. Thus, our data show that pancreatic islets in HD patients appear histologically normal. Functional studies of HD patients with respect to insulin secretion and islet function are required to elucidate the pathogenesis of DM in HD. This may lead to a better understanding of HD and provide novel therapeutic targets for symptomatic treatment in HD.


  • Diabetes - Molecular Metabolism
  • Department of Experimental Medical Science
  • Translational Neuroendocrinology
  • Pathology, Malmö

Publishing year







Histochemistry and Cell Biology



Document type

Journal article




  • Cell and Molecular Biology



Research group

  • Diabetes - Molecular Metabolism
  • Translational Neuroendocrinology
  • Pathology, Malmö


  • ISSN: 1432-119X