ArticleDiabetes2024
The Longitudinal Effect of Diabetes-Associated Variation in TCF7L2 on Islet Function in Humans.
Article in Diabetes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed.
- Hepatic steatosis in humans is associated with preserved glucagon action on amino acid metabolism.The Journal of clinical investigation · 2026Trial
- Converging TCF7L2 and CDKAL1 pathways in the pathogenesis of type 2 diabetes mellitus.Acta diabetologica · 2026Review
- Modeling the effect of glucagon on endogenous glucose production in healthy individuals under meal-like conditions.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
- Pharmacogenomics of Tirzepatide: Genomic Insights into Dual GIP/GLP-1 Agonist Response in Type 2 Diabetes and Atherosclerosis.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Abnormal Glucagon Secretion Contributes to a Longitudinal Decline in Glucose Tolerance.The Journal of clinical endocrinology and metabolism · 2025Observational
- Impact of TCF7L2 rs7903146 on clinical presentation and risk of complications in patients with type 2 diabetes.Diabetes, obesity & metabolism · 2025Article
- Enhanced quantification of α-cell suppression by hyperglycemia using a high-sensitivity glucagon assay.American journal of physiology. Endocrinology and metabolism · 2025Article
- The research progress and future directions in the pathophysiological mechanisms of type 2 diabetes mellitus from the perspective of precision medicine.Frontiers in medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
The T allele at rs7903146 in TCF7L2 increases the rate of conversion from prediabetes to type 2 diabetes. This has been associated with impaired β-cell function and with defective suppression of α-cell secretion by glucose. However, the temporal relationship of these abnormalities is uncertain. To study the longitudinal changes in islet function, we recruited 128 subjects, with 67 homozygous for the diabetes-associated allele (TT) at rs7903146 and 61 homozygous for the protective allele. Subjects were studied on two occasions, 3 years apart, using an oral 75-g glucose challenge. The oral minimal model was used to quantitate β-cell function; the glucagon secretion rate was estimated from deconvolution of glucagon concentrations. Glucose tolerance worsened in subjects with the TT genotype. This was accompanied by impaired postchallenge glucagon suppression but appropriate β-cell responsivity to rising glucose concentrations. These data suggest that α-cell abnormalities associated with the TT genotype (rs7903146) occur early and may precede β-cell dysfunction in people as they develop glucose intolerance and type 2 diabetes. ARTICLE HIGHLIGHTS:
Indexed as
Identifiers
What Socratic 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 Socratic graph.