ArticleDiabetes2016
Diabetes-Associated Variation in TCF7L2 Is Not Associated With Hepatic or Extrahepatic Insulin Resistance.
Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Insulin secretion and action and the response of endogenous glucose production to a lack of glucagon suppression in nondiabetic subjects.American journal of physiology. Endocrinology and metabolism · 2021Trial
- Diabetes-associated genetic variation in TCF7L2 alters pulsatile insulin secretion in humans.JCI insight · 2020Trial
- 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
- Abnormal Glucagon Secretion Contributes to a Longitudinal Decline in Glucose Tolerance.The Journal of clinical endocrinology and metabolism · 2025Observational
- The Longitudinal Effect of Diabetes-Associated Variation in TCF7L2 on Islet Function in Humans.Diabetes · 2024Article
- The Effect of Glucagon-Like Peptide 1 Receptor Blockade on Glucagon-Induced Stimulation of Insulin Secretion.Diabetes · 2023Article
- The Effect of Diabetes-Associated Variation inMetabolic syndrome and related disorders · 2022Article
- The T allele of TCF7L2 rs7903146 is associated with decreased glucose tolerance after bed rest in healthy older adults.Scientific reports · 2022Article
- Insulin Pulse Characteristics and Insulin Action in Non-diabetic Humans.The Journal of clinical endocrinology and metabolism · 2021Article
- Assessment of individual and standardized glucagon kinetics in healthy humans.American journal of physiology. Endocrinology and metabolism · 2021Article
- Diabetes as a risk factor for Alzheimer's disease in the Middle East and its shared pathological mediators.Saudi journal of biological sciences · 2020Review
- Assessment of pulsatile insulin secretion derived from peripheral plasma C-peptide concentrations by nonparametric stochastic deconvolution.American journal of physiology. Endocrinology and metabolism · 2019Article
- What Can Diabetes-Associated Genetic Variation in TCF7L2 Teach Us About the Pathogenesis of Type 2 Diabetes?Metabolic syndrome and related disorders · 2018Review
- Performance of individually measured vs population-based C-peptide kinetics to assess β-cell function in the presence and absence of acute insulin resistance.Diabetes, obesity & metabolism · 2018Article
- Impaired Insulin Action Is Associated With Increased Glucagon Concentrations in Nondiabetic Humans.The Journal of clinical endocrinology and metabolism · 2018Article
- The rs7903146 Variant in theDiabetes care · 2017Article
- Obstacles to Translating Genotype-Phenotype Correlates in Metabolic Disease.Physiology (Bethesda, Md.) · 2017Review
- Mechanisms Underlying the Pathogenesis of Isolated Impaired Glucose Tolerance in Humans.The Journal of clinical endocrinology and metabolism · 2016Article
- TCF7L2 polymorphism is associated with low nitric oxide release, endothelial dysfunction and enhanced inflammatory response after myocardial infarction.BBA clinical · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
A common genetic variation in TCF7L2 is associated with type 2 diabetes. However, the mechanism by which this occurs remains elusive. In addition to affecting insulin secretion, genetic variation at the TCF7L2 locus may alter insulin action or directly modify hepatic glucose metabolism. We sought to determine whether the diabetes-associated variant in this locus (the T allele of rs7903146) increases fasting endogenous glucose production (EGP), and impairs insulin-induced suppression of EGP and insulin-stimulated glucose disappearance. To address this, we studied individuals who were either homozygous for the diabetes-associated allele (TT) at rs7903146 or were homozygous for the protective allele (CC). Subjects were matched for other anthropometric characteristics and were studied using a euglycemic clamp. EGP and glucose uptake were measured using the tracer dilution technique, and the relative contribution of gluconeogenesis to EGP was quantitated using deuterated water corrected for transaldolase exchange. We report that the diabetes-associated variation in TCF7L2 did not associate with fasting EGP, insulin-induced suppression of EGP, and insulin-induced stimulation of glucose uptake. There was no association with the contribution of gluconeogenesis and glycogenolysis to EGP. These data indicate that genetic variation at TCF7L2 does not predispose an individual to type 2 diabetes by altering either hepatic or extrahepatic insulin action.
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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.