ReviewCureus2026
Impact of Core Circadian Gene Variants on Glycemic Parameters and Insulin Resistance in Type 2 Diabetes: A Systematic Review.
Review in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Circadian rhythm disruption is increasingly implicated in the pathophysiology of type 2 diabetes mellitus (T2DM). Variants in core circadian clock genes - CLOCK (circadian locomotor output cycles kaput), BMAL1/ARNTL (brain and muscle ARNT-like protein 1), CRY1/2 (cryptochrome 1 and 2), PER1-3 (period 1-3), and NR1D1 (REV-ERBα) - and associated melatonin receptor genes may influence glycaemic homeostasis and insulin resistance. This systematic review synthesises evidence published between 2020 and 2025 on associations between these variants and key glycaemic parameters. A systematic search of PubMed/MEDLINE, Embase, Web of Science, and the Cochrane Library was performed following PRISMA 2020 (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. Studies published from January 2020 to December 2025 that examined circadian gene variants or expression in T2DM or at-risk human populations and reported glycaemic or insulin-resistance outcomes were included. Risk of bias was independently assessed using the Newcastle-Ottawa Scale (NOS). Owing to substantial heterogeneity, a narrative synthesis following the Synthesis Without Meta-analysis (SWiM) framework was undertaken; no meta-analysis, formal heterogeneity (I²) metric, or GRADE certainty rating was performed. Six studies of diverse design (case control, cross-sectional, narrative review, and systematic review with meta-analysis) from China, South Africa, Croatia/multi-ethnic, and Spain, collectively involving more than 18,000 participants, met the inclusion criteria. A CLOCK rs1801260 × MTNR1A rs2119882 gene-gene interaction, CRY2 rs11605924, and BMAL1 rs3789327 were significantly associated with elevated fasting plasma glucose (FPG), higher Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), and increased T2DM risk. Reduced expression of core clock genes (BMAL1, CRY1, and PER2) correlated negatively with glycated haemoglobin (HbA1c) and HOMA-IR. BMAL1 rs7950226 was confirmed as a metabolic-syndrome susceptibility variant. Across 2020-2025, circadian gene variants were consistently associated with impaired glycaemic control and insulin resistance in T2DM. Because the available evidence is observational and heterogeneous, these findings suggest potential value in incorporating circadian genetic profiling into precision diabetes risk stratification rather than established causal utility, and prospective validation is required.
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Registered trials
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.