ReviewDiabetes, metabolic syndrome and obesity : targets and therapy2024
Evaluating the Overall Safety of Glucokinase Activators in Patients with Type 2 Diabetes Mellitus.
Review in Diabetes, metabolic syndrome and obesity : targets and therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed.
- Contrasting Effects of Chronic Glucokinase Activation and Inhibition on Pancreatic Beta-Cell Function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- TAT-PBX1 Reverses Hyperglycemia Through β-Cell Regeneration and Functional Restoration in an STZ-Induced Diabetic Model.Pharmaceuticals (Basel, Switzerland) · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: This study aimed to assess the overall clinical adverse events (AEs) associated with glucokinase activators (GKAs) in patients with type 2 diabetes mellitus (T2DM). Methods: We searched MEDLINE, EMBASE, Cochrane Library, and ClinicalTrials.gov databases from their dates of inception to June 6, 2023, for randomized controlled trials (RCTs) that reported safety data for GKAs in patients with T2DM. A random-effects model was used to obtain a summary odds ratio (OR) with associated 95% Confidence Intervals (CIs). Pre-specified subgroup analyses were conducted according to individual GKAs (dorzagliatin and all other GKAs), various controls, follow-up duration, mean duration of diabetes, and the location of clinical research. Results: 17 RCTs enrolling 4,918 patients (3,196 patients received GKAs and 1,722 patients received placebo or other hypoglycemic drugs) were identified. Among the 17 RCTs, dorzagliatin, AZD1656 and MK-0941 in three trials (1,541 patients), five trials (885 patients), and three trials (798 patients), respectively. GKA treatment was associated with a higher risk of any AEs (OR 1.220, 95% CI 1.072-1.389), mild AEs (OR 1.373, 95% CI 1.085-1.738), hyperlipidemia (OR 1.532, 95% CI 1.071-2.189), and hyperuricemia (OR 2.768, 95% CI 1.562-4.903) compared to patients in the control groups. The higher risks of any AEs were mainly attributed to dorzagliatin and MK-0941 and mild AEs mainly attributed to dorzagliatin. Notably, dorzagliatin had significant effects on the occurrence of hyperlipidemia (OR 1.476, 95% CI 1.025-2.126) and hyperuricemia (OR 2.727, 95% CI 1.523-4.883) in the subgroup analyses. No significant effects were detected from other GKAs when regarding hyperlipidemia and hyperuricemia. Conclusion: The results of our meta-analysis indicated that GKAs were associated with a higher risk of any AEs, mild AEs, hyperlipidemia, and hyperuricemia. Further subgroup analyses revealed that the increased occurrence of hyperlipidemia, and hyperuricemia mainly originated from dorzagliatin treatment.
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