ArticleJournal of diabetes2023
β-Cell glucokinase expression was increased in type 2 diabetes subjects with better glycemic control.
Article in Journal of diabetes, 2023. 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, 16 citations in OpenAlex.
- Factors influencing the initial glycemic efficacy of dorzagliatin, a novel glucokinase activator, in type 2 diabetes.Endocrine · 2025Article
- β-Cell Dedifferentiation in HOMA-βlow and HOMA-βhigh Subjects.The Journal of clinical endocrinology and metabolism · 2025Article
- Identification of Novel Genetic Variants and Food Intake Factors Associated with Type 2 Diabetes in South Korean Adults, Using an Illness-Death Model.International journal of molecular sciences · 2025Article
- Molecular Docking, Pharmacophore Modeling and ADMET Prediction of Novel Heterocyclic Leads as Glucokinase Activators.Anti-inflammatory & anti-allergy agents in medicinal chemistry · 2025Article
- Clinical investigation of glucokinase activators for the restoration of glucose homeostasis in diabetes.Journal of diabetes · 2024Review
- Prediction of Protein-Drug Interactions, Pharmacophore Modeling, and Toxicokinetics of Novel Leads for Type 2 Diabetes Treatment.Current drug metabolism · 2024Article
- New-Generation Glucokinase Activators: Potential Game-Changers in Type 2 Diabetes Treatment.International journal of molecular sciences · 2024Review
- β-Cell glucokinase expression was increased in type 2 diabetes subjects with better glycemic control.Journal of diabetes · 2023Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundType 2 diabetes (T2D) is characterized by a progressive deterioration of β-cell function with a continuous decline in insulin secretion. Glucokinase (GCK) facilitates the rate-limiting step of glycolysis in pancreatic β-cells, to acquire the proper glucose-stimulated insulin secretion. Multiple glucokinase activators (GKAs) have been developed and clinically tested. However, the dynamic change of human pancreatic GCK expression during T2D progression has not been investigated.
methodsWe evaluated GCK expression by measuring the average immunoreactivity of GCK in insulin
resultsWe did not detect changes of GCK expression in IFG islets. However, we found β-cell GCK levels were significantly increased in T2D with adequate glucose control (wT2D) but not in T2D with poor glucose control (uT2D). Furthermore, there was a strong positive correlation between GCK expression and adaptive UPR (spliced X-box binding protein 1 [XBP1s] and activating transcription factor 4 [ATF4]), as well as functional maturity marker (urocortin-3 [UCN3]) in human diabetic β-cells.
conclusionsOur study demonstrates that inductions of GCK enhanced adaptive UPR and UCN3 in human β-cells, which might be an adaptive mechanism during T2D progression. This finding provides a rationale for exploring novel molecules that activate β-cell GCK and thereby improve pharmacological treatment of T2D.
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