ArticleNature communications2024
Diabetic sensory neuropathy and insulin resistance are induced by loss of UCHL1 in Drosophila.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Metabolic regulation of calcium homeostasis via SERCA succination.Science advances · 2026Article
- Review
- Mosaic partial epidermal reprogramming remodels neighbors and niches to refine skin homeostasis and repair.Nature communications · 2026Article
- Ubiquitination modifications as central regulators of metabolic dysfunction in type 2 diabetes mellitus.Frontiers in endocrinology · 2026Review
- Novel three-dimensional analysis method for accurate evaluation of cutaneous small sensory nerve fibers in mice.Journal of toxicologic pathology · 2025Article
- The relevance of combined testing of cerebrospinal fluid glial fibrillary acidic protein and ubiquitin C-terminal hydrolase L1 in multiple sclerosis and peripheral neuropathy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Article
- Identification of key ubiquitination-related genes in gestational diabetes mellitus: A bioinformatics-driven study.Health science reports · 2024Article
- Identification of the Shared Gene Signatures Between Alzheimer's Disease and Diabetes-Associated Cognitive Dysfunction by Bioinformatics Analysis Combined with Biological Experiment.Journal of Alzheimer's disease : JAD · 2024Article
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Authors and funding
10 authors at 2 institutions in 3 countries.
Funding
Abstract
Diabetic sensory neuropathy (DSN) is one of the most common complications of type 2 diabetes (T2D), however the molecular mechanistic association between T2D and DSN remains elusive. Here we identify ubiquitin C-terminal hydrolase L1 (UCHL1), a deubiquitinase highly expressed in neurons, as a key molecule underlying T2D and DSN. Genetic ablation of UCHL1 leads to neuronal insulin resistance and T2D-related symptoms in Drosophila. Furthermore, loss of UCHL1 induces DSN-like phenotypes, including numbness to external noxious stimuli and axonal degeneration of sensory neurons in flies' legs. Conversely, UCHL1 overexpression improves DSN-like defects of T2D model flies. UCHL1 governs insulin signaling by deubiquitinating insulin receptor substrate 1 (IRS1) and antagonizes an E3 ligase of IRS1, Cullin 1 (CUL1). Consistent with these results, genetic and pharmacological suppression of CUL1 activity rescues T2D- and DSN-associated phenotypes. Therefore, our findings suggest a complete set of genetic factors explaining T2D and DSN, together with potential remedies for the diseases.
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