ArticleThe Journal of biological chemistry
NGBR is required to ameliorate type 2 diabetes in mice by enhancing insulin sensitivity.
Article in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- From Molecules to Biomarkers: Nogo Proteins and Receptors in the Early Detection of Type 2 Diabetes Complications: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Mitochondria-endoplasmic reticulum-lipid droplet crosstalk in lipid metabolic reprogramming in type 2 diabetes mellitus.Journal of lipid research · 2026Review
- Impaired glycosylation promotes rapid transition to hepatocellular carcinoma in model of diet-induced steatotic liver disease.The Journal of clinical investigation · 2026Article
- Endoplasmic reticulum stress in skeletal muscle dysfunction of type 2 diabetes: mechanisms and therapeutic implications.Frontiers in endocrinology · 2026Review
- The Progression of NUS1-Associated Parkinson's Disease and the Diagnostic Potential of Plasma NgBR.CNS neuroscience & therapeutics · 2025Article
- Review
- NUS1 Variants Cause Lennox-Gastaut Syndrome Related to Unfolded Protein Reaction Activation.Molecular neurobiology · 2024Article
- Intestinal Nogo-B reduces GLP1 levels by binding to proglucagon on the endoplasmic reticulum to inhibit PCSK1 cleavage.Nature communications · 2024Article
- Comprehensive insights into berberine's hypoglycemic mechanisms: A focus on ileocecal microbiome in db/db mice.Heliyon · 2024Article
- Impact of Lipids on Insulin Resistance: Insights from Human and Animal Studies.Drug design, development and therapy · 2024Review
- Loss of cis-PTase function in the liver promotes a highly penetrant form of fatty liver disease that rapidly transitions to hepatocellular carcinoma.bioRxiv : the preprint server for biology · 2023Article
- Hypoglycemic mechanisms ofHeliyon · 2023Article
- Activatable "Matryoshka" nanosystem delivery NgBR siRNA and control drug release for stepwise therapy and evaluate drug resistance cancer.Materials today. Bio · 2022Article
- Shared genetic mechanism between type 2 diabetes and COVID-19 using pathway-based association analysis.Frontiers in genetics · 2022Article
- Peroxisome Proliferator-Activated Receptor-Gamma Reduces ER Stress and Inflammation via Targeting NGBR Expression.Frontiers in pharmacology · 2021Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The reduction of insulin resistance or improvement of insulin sensitivity is the most effective treatment for type 2 diabetes (T2D). We previously reported that Nogo-B receptor (NGBR), encoded by the NUS1 gene, is required for attenuating hepatic lipogenesis by blocking nuclear translocation of liver X receptor alpha, suggesting its important role in regulating hepatic lipid metabolism. Herein, we demonstrate that NGBR expression was decreased in the liver of obesity-associated T2D patients and db/db mice. NGBR knockout in mouse hepatocytes resulted in increased blood glucose, insulin resistance, and beta-cell loss. High-fat diet (HFD)/streptozotocin (STZ)-treated mice presented the T2D phenotype by showing increased nonesterified fatty acid (NEFA) and triglyceride (TG) in the liver and plasma and increased insulin resistance and beta-cell loss. AAV-mediated NGBR overexpression in the liver reduced NEFA and TG in the liver and circulation and improved liver functions. Consequently, HFD/STZ-treated mice with hepatic NGBR overexpression had increased insulin sensitivity and reduced beta-cell loss. Mechanistically, NGBR overexpression restored insulin signaling of AMPKα1-dependent phosphorylation of AKT and GSK3β. NGBR overexpression also reduced expression of endoplasmic reticulum stress-associated genes in the liver and skeletal muscle to improve insulin sensitivity. Together, our results reveal that NGBR is required to ameliorate T2D in mice, providing new insight into the role of hepatic NGBR in insulin sensitivity and T2D treatment.
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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.