ArticleMechanisms of ageing and development2025
Transcriptomic and epigenomic signatures of liver metabolism and insulin sensitivity in aging mice.
Article in Mechanisms of ageing and development, 2025. 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.
- Single-cell and spatial omics in liver identify cell-cell communication regulators in aging and insulin resistance.Metabolism: clinical and experimental · 2026Article
- Preliminary Metabolomic Analysis: Serum Metabolomic Dynamics During Estrus Synchronization in Kazakh Mares.Animals : an open access journal from MDPI · 2026Article
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
Abstract
Age-related declines in insulin sensitivity and glucose metabolism contribute to metabolic disease. Despite the liver's central role in glucose homeostasis, a comprehensive phenotypic characterization and concurrent molecular analysis of insulin resistance and metabolic dysfunction in the aging liver is lacking. We characterized hepatic insulin resistance and mitochondrial metabolic defects through metabolic cage, hyperinsulinemic-euglycemic clamp, and tracer studies paired with transcriptomic and DNA methylation analyses in young and aged male mice. Aged mice exhibited benchmark measures of whole body and liver insulin resistance. Aged mice showed lower pyruvate dehydrogenase flux, decreased fatty acid oxidation and citrate synthase fluxes, and increased pyruvate carboxylase flux under insulin-stimulated conditions. Molecular analysis revealed age-related changes in metabolic genes Pck1, Socs3, Tbc1d4, and Enpp1. Unsupervised network analysis identified an intercorrelated phenotype module (ME-Glucose), RNA module, and DNA methylation module. The DNA methylation module was enriched for lipid metabolism pathways and TCF-1 binding, while the RNA module was enriched for MZF-1 binding and regulation by miR-155-5p. Protein-protein interaction network analysis revealed interactions between module genes and canonical metabolic pathways, highlighting genes including Ets1, Ppp1r3b, and Enpp3. This study reveals novel genes underlying age-related hepatic insulin resistance as potential targets for metabolic interventions to promote healthy aging.
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.