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

Bacos, Karl LU orcid ; Björkqvist, Maria LU orcid ; Petersén, Åsa LU ; Luts, Lena LU ; Maat-Schieman, Marion ; Roos, Raymund ; Sundler, Frank LU ; Brundin, Patrik LU ; Mulder, Hindrik LU orcid and Wierup, Nils LU (2008) In Histochemistry and Cell Biology 129. p.623-629
Abstract
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... (More)
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. (Less)
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author
; ; ; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Histochemistry and Cell Biology
volume
129
pages
623 - 629
publisher
Springer
external identifiers
  • pmid:18259770
  • wos:000255091700008
  • scopus:42449153671
ISSN
1432-119X
DOI
10.1007/s00418-008-0393-z
language
English
LU publication?
yes
id
0f554f3f-f93b-41b8-9a59-e648bd247bb2 (old id 1042132)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/18259770?dopt=Abstract
date added to LUP
2016-04-04 08:55:28
date last changed
2023-09-05 17:54:52
@article{0f554f3f-f93b-41b8-9a59-e648bd247bb2,
  abstract     = {{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.}},
  author       = {{Bacos, Karl and Björkqvist, Maria and Petersén, Åsa and Luts, Lena and Maat-Schieman, Marion and Roos, Raymund and Sundler, Frank and Brundin, Patrik and Mulder, Hindrik and Wierup, Nils}},
  issn         = {{1432-119X}},
  language     = {{eng}},
  pages        = {{623--629}},
  publisher    = {{Springer}},
  series       = {{Histochemistry and Cell Biology}},
  title        = {{Islet beta-cell area and hormone expression are unaltered in Huntington's disease.}},
  url          = {{http://dx.doi.org/10.1007/s00418-008-0393-z}},
  doi          = {{10.1007/s00418-008-0393-z}},
  volume       = {{129}},
  year         = {{2008}},
}