ArticleHistochemistry and cell biology2008
Islet beta-cell area and hormone expression are unaltered in Huntington's disease.
Article in Histochemistry and cell biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 31 citations in OpenAlex.
- Concomitant pathologies and their impact on Huntington's disease. A brief review of current evidence.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Potential molecular mechanism of exercise reversing insulin resistance and improving neurodegenerative diseases.Frontiers in physiology · 2024Review
- Metabolism in Huntington's disease: a major contributor to pathology.Metabolic brain disease · 2022Review
- Movement Disorders and the Gut: A Review.Movement disorders clinical practice · 2022Review
- Glycation in Huntington's Disease: A Possible Modifier and Target for Intervention.Journal of Huntington's disease · 2019Review
- Huntington's Disease and Diabetes: Chronological Sequence of its Association.Journal of Huntington's disease · 2017Review
- Mechanisms of action of brain insulin against neurodegenerative diseases.Journal of neural transmission (Vienna, Austria : 1996) · 2014Review
- Pancreatic diabetes manifests when beta cell area declines by approximately 65% in humans.Diabetologia · 2012Article
- Formation of polyglutamine inclusions in a wide range of non-CNS tissues in the HdhQ150 knock-in mouse model of Huntington's disease.PloS one · 2009Article
- State-of-the-art technologies, current opinions and developments, and novel findings: news from the field of histochemistry and cell biology.Histochemistry and cell biology · 2008Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.