ArticleDiabetes2015
Dietary iron controls circadian hepatic glucose metabolism through heme synthesis.
Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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Who cites it
32 citing papers in PubMed, 54 citations in OpenAlex.
- Tissue Iron Predicts Metformin Responsiveness in a Mouse Model and in Humans with Type 2 Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
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- Redox status regulates eggshell color by modulating protoporphyrin IX biosynthesis via the SIRT1/PGC-1α/ALAS1 axis in brown-shelled hens.Journal of animal science and biotechnology · 2025Article
- Iron homeostasis and ferroptosis in human diseases: mechanisms and therapeutic prospects.Signal transduction and targeted therapy · 2024Review
- Remnant cholesterol, iron status and diabetes mellitus: a dose-response relationship and mediation analysis.Diabetology & metabolic syndrome · 2024Article
- Cellular iron depletion enhances behavioral rhythm by limiting brain Per1 expression in mice.CNS neuroscience & therapeutics · 2024Article
- Characteristics of insulin resistance in Korean adults from the perspective of circadian and metabolic sensing genes.Genes & genomics · 2023Article
- Iron, glucose and fat metabolism and obesity: an intertwined relationship.International journal of obesity (2005) · 2023Review
- Iron metabolism and ferroptosis in type 2 diabetes mellitus and complications: mechanisms and therapeutic opportunities.Cell death & disease · 2023Review
- Iron and the Pathophysiology of Diabetes.Annual review of physiology · 2023Review
- Modulating Glycolysis to Improve Cancer Therapy.International journal of molecular sciences · 2023Review
- Therapy Follows Diagnosis: Old and New Approaches for the Treatment of Acute Porphyrias, What We Know and What We Should Know.Diagnostics (Basel, Switzerland) · 2022Review
- Iron accumulation with age alters metabolic pattern and circadian clock gene expression through the reduction of AMP-modulated histone methylation.The Journal of biological chemistry · 2022Article
- Melatonin: Regulation of Prion Protein Phase Separation in Cancer Multidrug Resistance.Molecules (Basel, Switzerland) · 2022Review
- Multi-Modal Regulation of Circadian Physiology by Interactive Features of Biological Clocks.Biology · 2021Review
- An Analysis of the Multifaceted Roles of Heme in the Pathogenesis of Cancer and Related Diseases.Cancers · 2021Review
- Prediction and analysis of metagenomic operons via MetaRon: a pipeline for prediction of Metagenome and whole-genome opeRons.BMC genomics · 2021Article
- Proinflammatory Cytokines Perturb Mouse and Human Pancreatic Islet Circadian Rhythmicity and Induce Uncoordinated β-Cell Clock Gene Expression via Nitric Oxide, Lysine Deacetylases, and Immunoproteasomal Activity.International journal of molecular sciences · 2020Article
- Targeting REV-ERBα for therapeutic purposes: promises and challenges.Theranostics · 2020Review
- Evidence that genes involved in hedgehog signaling are associated with both bipolar disorder and high BMI.Translational psychiatry · 2019Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
The circadian rhythm of the liver maintains glucose homeostasis, and disruption of this rhythm is associated with type 2 diabetes. Feeding is one factor that sets the circadian clock in peripheral tissues, but relatively little is known about the role of specific dietary components in that regard. We assessed the effects of dietary iron on circadian gluconeogenesis. Dietary iron affects circadian glucose metabolism through heme-mediated regulation of the interaction of nuclear receptor subfamily 1 group d member 1 (Rev-Erbα) with its cosuppressor nuclear receptor corepressor 1 (NCOR). Loss of regulated heme synthesis was achieved by aminolevulinic acid (ALA) treatment of mice or cultured cells to bypass the rate-limiting enzyme in hepatic heme synthesis, ALA synthase 1 (ALAS1). ALA treatment abolishes differences in hepatic glucose production and in the expression of gluconeogenic enzymes seen with variation of dietary iron. The differences among diets are also lost with inhibition of heme synthesis with isonicotinylhydrazine. Dietary iron modulates levels of peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), a transcriptional activator of ALAS1, to affect hepatic heme. Treatment of mice with the antioxidant N-acetylcysteine diminishes PGC-1α variation observed among the iron diets, suggesting that iron is acting through reactive oxygen species signaling.
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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.