Trial reportBMJ open diabetes research & care2023
Can earlier biomarker measurements explain a treatment effect on diabetes incidence? A robust comparison of five surrogate markers.
Trial report in BMJ open diabetes research & care, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed, 2 citations in OpenAlex.
- Insulin Resistance as a Systemic Metabolic Risk State for Cancer: Mechanisms, Biomarkers, and Prevention.International journal of molecular sciences · 2026Review
- Bedside implications of the use of surrogate endpoints in solid and haematological cancers: implications for our reliance on PFS, DFS, ORR, MRD and more.BMJ oncology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
introductionWe measured and compared five individual surrogate markers-change from baseline to 1 year after randomization in hemoglobin A1c (HbA1c), fasting glucose, 2-hour postchallenge glucose, triglyceride-glucose index (TyG) index, and homeostatic model assessment of insulin resistance (HOMA-IR)-in terms of their ability to explain a treatment effect on reducing the risk of type 2 diabetes mellitus at 2, 3, and 4 years after treatment initiation. RESEARCH DESIGN AND
methodsStudy participants were from the Diabetes Prevention Program study, randomly assigned to either a lifestyle intervention (n=1023) or placebo (n=1030). The surrogate markers were measured at baseline and 1 year, and diabetes incidence was examined at 2, 3, and 4 years postrandomization. Surrogacy was evaluated using a robust model-free estimate of the proportion of treatment effect explained (PTE) by the surrogate marker.
resultsAcross all time points, change in fasting glucose and HOMA-IR explained higher proportions of the treatment effect than 2-hour glucose, TyG index, or HbA1c. For example, at 2 years, glucose explained the highest (80.1%) proportion of the treatment effect, followed by HOMA-IR (77.7%), 2-hour glucose (76.2%), and HbA1c (74.6%); the TyG index explained the smallest (70.3%) proportion.
conclusionsThese data suggest that, of the five examined surrogate markers, glucose and HOMA-IR were the superior surrogate markers in terms of PTE, compared with 2-hour glucose, HbA1c, and TyG index.
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What OpenQuestion holds
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.