ArticleInternational journal of biological sciences2012
Reduction in Tcf7l2 expression decreases diabetic susceptibility in mice.
Article in International journal of biological sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 33 citations in OpenAlex.
- Review
- Differential chromatin accessibility and Gene Expression Associated with Backfat Deposition in pigs.BMC genomics · 2024Article
- Tcf7l2 in hepatocytes regulates de novo lipogenesis in diet-induced non-alcoholic fatty liver disease in mice.Diabetologia · 2023Article
- Combined effect of pancreatic lipid content and gene variants (TCF7L2, WFS1 and 11BHSD1) on B-cell function in Middle Aged Women in a Post Hoc Analysis.Diabetology & metabolic syndrome · 2022Article
- Triazole-Based Inhibitors of the Wnt/β-Catenin Signaling Pathway Improve Glucose and Lipid Metabolisms in Diet-Induced Obese Mice.Journal of medicinal chemistry · 2019Article
- What Can Diabetes-Associated Genetic Variation in TCF7L2 Teach Us About the Pathogenesis of Type 2 Diabetes?Metabolic syndrome and related disorders · 2018Review
- A high throughput, functional screen of human Body Mass Index GWAS loci using tissue-specific RNAi Drosophila melanogaster crosses.PLoS genetics · 2018Article
- The Diabetes Gene and Wnt Pathway Effector TCF7L2 Regulates Adipocyte Development and Function.Diabetes · 2018Article
- The Wnt Signaling Pathway Effector TCF7L2 Mediates Olanzapine-Induced Weight Gain and Insulin Resistance.Frontiers in pharmacology · 2018Article
- Rare intronic variants of TCF7L2 arising by selective sweeps in an indigenous population from Mexico.BMC genetics · 2016Article
- Evidence of non-pancreatic beta cell-dependent roles of Tcf7l2 in the regulation of glucose metabolism in mice.Human molecular genetics · 2015Article
- TCF7L2 is a master regulator of insulin production and processing.Human molecular genetics · 2014Article
- TCF7L2 in mouse pancreatic beta cells plays a crucial role in glucose homeostasis by regulating beta cell mass.Diabetologia · 2014Article
- Article
- Animal models of GWAS-identified type 2 diabetes genes.Journal of diabetes research · 2013Review
- From mice to humans.Current diabetes reports · 2012Review
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 1 institution in 1 country.
Funding
Abstract
objectiveThe WNT signaling pathway effector gene TCF7L2 has been associated with an increased risk of type 2 diabetes. However, it remains unclear how this gene affects diabetic pathogenesis. The goal of this study was to investigate the effects of Tcf7l2 haploinsufficiency on metabolic phenotypes in mice. EXPERIMENTAL
designTcf7l2 knockout (Tcf7l⁻/⁻) mice were generated. Because of the early mortality of Tcf7l2⁻/⁻ mice, we characterized the metabolic phenotypes of heterozygous Tcf7l2⁺/⁻ mice in comparison to the wild-type controls. The mice were fed a normal chow diet or a high fat diet (HFD) for 9 weeks.
resultsThe Tcf7l2⁺/⁻ mice showed significant differences from the wild-type mice with regards to body weight, fasting glucose and insulin levels. Tcf7l2⁺/⁻ mice displayed improved glucose tolerance. In the liver of Tcf7l2⁺/⁻ mice fed on the HFD, reduced lipogenesis and hepatic triglyceride levels were observed when compared with those of wild-type mice. Furthermore, the Tcf7l2⁺/⁻ mice fed on the HFD exhibited decreased peripheral fat deposition. Immunohistochemistry in mouse pancreatic islets showed that endogenous expression of Tcf7l2 was upregulated in the wild-type mice, but not in the Tcf7l2⁺/⁻ mice, after feeding with the HFD. However, the haploinsufficiency of Tcf7l2 in mouse pancreatic islets resulted in little changes in glucose-stimulated insulin secretion.
conclusionThese results suggest that decreased expression of Tcf7l2 confers reduction of diabetic susceptibility in mice via regulation on the metabolism of glucose and lipid.
Indexed as
Identifiers
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.