Islet beta-cell area and hormone expression are unaltered in Huntington's disease.
Författare
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.
Avdelning/ar
Publiceringsår
2008
Språk
Engelska
Sidor
623-629
Publikation/Tidskrift/Serie
Histochemistry and Cell Biology
Volym
129
Länkar
Dokumenttyp
Artikel i tidskrift
Förlag
Springer
Ämne
- Cell and Molecular Biology
Status
Published
Forskningsgrupp
- Diabetes - Molecular Metabolism
- Translational Neuroendocrinology
- Pathology, Malmö
ISBN/ISSN/Övrigt
- ISSN: 1432-119X