ArticleScientific reports2019
Peripheral Expression of Mutant Huntingtin is a Critical Determinant of Weight Loss and Metabolic Disturbances in Huntington's Disease.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- PROTAC-Mediated Degradation of mHTT Aggregates Attenuates Neurotoxicity in Cellular and R6/2 Mouse Models of Huntington's Disease.Journal of the American Chemical Society · 2026Article
- Silent destruction: hidden muscle wasting and body decline in early Huntington's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2026Article
- Copy Number Variations in Short Tandem Repeats Modulate Growth Traits in Penaeid Shrimp Through Neighboring Gene Regulation.Animals : an open access journal from MDPI · 2025Article
- Metabolomics and lipidomics in pectus excavatum: preliminary screening of biomarkers for early diagnosis.Translational pediatrics · 2024Article
- Apoptosis Genes as a Key to Identification of Inverse Comorbidity of Huntington's Disease and Cancer.International journal of molecular sciences · 2023Article
- Tumor suppressor p53 regulates heat shock factor 1 protein degradation in Huntington's disease.Cell reports · 2023Article
- Vitamin B3 Biotech · 2023Article
- Progressive transcriptional changes in metabolic genes and altered fatbody homeostasis in Drosophila model of Huntington's disease.Metabolic brain disease · 2022Article
- Metabolism in Huntington's disease: a major contributor to pathology.Metabolic brain disease · 2022Review
- Alterations in the Gut Fungal Community in a Mouse Model of Huntington's Disease.Microbiology spectrum · 2022Article
- Rehabilitation outcomes in Huntington disease patients with low body mass index.Journal of musculoskeletal & neuronal interactions · 2022Article
- Systemic manifestation and contribution of peripheral tissues to Huntington's disease pathogenesis.Ageing research reviews · 2021Review
- Genetic Screen in Adult Drosophila Reveals That dCBP Depletion in Glial Cells Mitigates Huntington Disease Pathology through a Foxo-Dependent Pathway.International journal of molecular sciences · 2021Article
- Quantifying the Onset of Unintended Weight Loss in Huntington's Disease: A Retrospective Analysis of Enroll-HD.Journal of Huntington's disease · 2021Article
- Review
- Juvenile Huntington's Disease Skin Fibroblasts Respond with Elevated Parkin Level and Increased Proteasome Activity as a Potential Mechanism to Counterbalance the Pathological Consequences of Mutant Huntingtin Protein.International journal of molecular sciences · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deteriorating weight loss in patients with Huntington's disease (HD) is a complicated peripheral manifestation and the cause remains poorly understood. Studies suggest that body weight strongly influences the clinical progression rate of HD and thereby offers a valuable target for therapeutic interventions. Mutant huntingtin (mHTT) is ubiquitously expressed and could induce toxicity by directly acting in the peripheral tissues. We investigated the effects of selective expression of mHTT exon1 in fat body (FB; functionally equivalent to human adipose tissue and liver) using transgenic Drosophila. We find that FB-autonomous expression of mHTT exon1 is intrinsically toxic and causes chronic weight loss in the flies despite progressive hyperphagia, and early adult death. Moreover, flies exhibit loss of intracellular lipid stores, and decline in the systemic levels of lipids and carbohydrates which aggravates over time, representing metabolic defects. At the cellular level, besides impairment, cell death also occurs with the formation of mHTT aggregates in the FB. These findings indicate that FB-autonomous expression of mHTT alone is sufficient to cause metabolic abnormalities and emaciation in vivo without any neurodegenerative cues.
Indexed as
Identifiers
What OpenQuestion holds
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.