ArticleThe Journal of biological chemistry2012
Euglycemic agent-mediated hypothalamic transcriptomic manipulation in the N171-82Q model of Huntington disease is related to their physiological efficacy.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- The promise of GLP-1 receptor agonists for neurodegenerative diseases.The Journal of clinical investigation · 2026Review
- Neurotrophins as Potential Gene Therapy Targets for Huntington's Disease.Current gene therapy · 2025Review
- Metabolism in Huntington's disease: a major contributor to pathology.Metabolic brain disease · 2022Review
- Exendin-4 alleviates β-Amyloid peptide toxicityFrontiers in aging neuroscience · 2022Article
- GPCRs Are Optimal Regulators of Complex Biological Systems and Orchestrate the Interface between Health and Disease.International journal of molecular sciences · 2021Review
- Insulin and Exendin-4 Reduced Mutated Huntingtin Accumulation in Neuronal Cells.Frontiers in pharmacology · 2020Article
- Glycation in Huntington's Disease: A Possible Modifier and Target for Intervention.Journal of Huntington's disease · 2019Review
- The Emerging Role of GLP-1 Receptors in DNA Repair: Implications in Neurological Disorders.International journal of molecular sciences · 2017Review
- Altered learning, memory, and social behavior in type 1 taste receptor subunit 3 knock-out mice are associated with neuronal dysfunction.The Journal of biological chemistry · 2017Article
- Neurodegeneration Alters Metabolic Profile and Sirt 1 Signaling in High-Fat-Induced Obese Mice.Molecular neurobiology · 2017Article
- Huntington's Disease and Diabetes: Chronological Sequence of its Association.Journal of Huntington's disease · 2017Review
- Informatic deconvolution of biased GPCR signaling mechanisms from in vivo pharmacological experimentation.Methods (San Diego, Calif.) · 2016Article
- Investigating the role of filamin C in Belgian patients with frontotemporal dementia linked to GRN deficiency in FTLD-TDP brains.Acta neuropathologica communications · 2015Article
- Delineation of a conserved arrestin-biased signaling repertoire in vivo.Molecular pharmacology · 2015Article
- Components of the endocannabinoid and dopamine systems are dysregulated in Huntington's disease: analysis of publicly available microarray datasets.Pharmacology research & perspectives · 2015Article
- Amitriptyline improves motor function via enhanced neurotrophin signaling and mitochondrial functions in the murine N171-82Q Huntington disease model.The Journal of biological chemistry · 2015Article
- GIT2 Acts as a Systems-Level Coordinator of Neurometabolic Activity and Pathophysiological Aging.Frontiers in endocrinology · 2015Article
- Longitudinal analysis of calorie restriction on rat taste bud morphology and expression of sweet taste modulators.The journals of gerontology. Series A, Biological sciences and medical sciences · 2014Article
- Systems-Level G Protein-Coupled Receptor Therapy Across a Neurodegenerative Continuum by the GLP-1 Receptor System.Frontiers in endocrinology · 2014Review
- Metabolic and hormonal signatures in pre-manifest and manifest Huntington's disease patients.Frontiers in physiology · 2014Article
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Authors and funding
11 authors at 2 institutions in 1 country.
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Abstract
Our aim was to employ novel analytical methods to investigate the therapeutic treatment of the energy regulation dysfunction occurring in a Huntington disease (HD) mouse model. HD is a neurodegenerative disorder that is characterized by progressive motor impairment and cognitive alterations. Changes in neuroendocrine function, body weight, energy metabolism, euglycemia, appetite function, and gut function can also occur. It is likely that the locus of these alterations is the hypothalamus. We determined the effects of three different euglycemic agents on HD progression using standard physiological and transcriptomic signature analyses. N171-82Q HD mice were treated with insulin, Exendin-4, and the newly developed GLP-1-Tf to determine whether these agents could improve energy regulation and delay disease progression. Blood glucose, insulin, metabolic hormone levels, and pancreatic morphology were assessed. Hypothalamic gene transcription, motor coordination, and life span were also determined. The N171-82Q mice exhibited significant alterations in hypothalamic gene transcription signatures and energy metabolism that were ameliorated, to varying degrees, by the different euglycemic agents. Exendin-4 or GLP-1-Tf (but not insulin) treatment also improved pancreatic morphology, motor coordination, and increased life span. Using hypothalamic transcription signature analyses, we found that the physiological efficacy variation of the drugs was evident in the degree of reversal of the hypothalamic HD pathological signature. Euglycemic agents targeting hypothalamic and energy regulation dysfunction in HD could potentially alter disease progression and improve quality of life in HD.
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