ArticleThe Journal of biological chemistry2012
NAD+-dependent sirtuin 1 and 6 proteins coordinate a switch from glucose to fatty acid oxidation during the acute inflammatory response.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 188 papers.
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Who cites it
188 citing papers in PubMed, 332 citations in OpenAlex.
- SIRT6 activator MDL-800 alleviates periodontal inflammation by inhibiting AIM2 pathway.Acta pharmaceutica Sinica. B · 2026Article
- Metabolic-epigenetic crosstalk in innate immune cell plasticity within the tumor microenvironment.Experimental & molecular medicine · 2026Review
- 3-Hydroxypropionic acid converts inflammatory macrophage glycolysis into mitochondrial oxidation through GAPDH carboxyethylation.iScience · 2026Article
- SIRT2 Regulates EX VIVO PBMC Adhesion in Septic Shock Patients.Shock (Augusta, Ga.) · 2026Article
- Sepsis and the immunometabolic inflammatory response.npj metabolic health and disease · 2026Review
- Recent perspectives on macrophage memory: types, mechanisms, and characteristics in pulmonary diseases.Cell communication and signaling : CCS · 2026Review
- The immunology of sepsis: translating new insights into clinical practice.Nature reviews. Nephrology · 2026Review
- The Effects of Exercise Combined with Pharmacotherapy on Body Composition and Metabolic Parameters in Overweight/Obese Adults: A Meta-Analysis and Network Pharmacology Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Cross-talk between lipopolysaccharide tolerance and AGEs in the regulation of macrophage inflammation and cholesterol efflux.Frontiers in immunology · 2026Article
- Metabolic and post-translational modifications in sepsis-associated immune dysfunction: a conceptual framework.Frontiers in immunology · 2026Review
- Interactions between Innate Immune Memory and the Central Nervous System.Neuroimmunomodulation · 2026Review
- Pyruvate Dehydrogenase Complex Stimulation With Dichloroacetate May Improve Septic Cardiac Dysfunction.Shock (Augusta, Ga.) · 2025Article
- Lactate metabolism is exploited bymBio · 2025Article
- Epigenetics and Mitochondrial Biogenesis: The Role of Sirtuins in HIV Neuropathogenesis.Molecular neurobiology · 2025Article
- Lipid metabolic adaptations during inflammation are controlled by the circadian clock and impaired by light at night.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Mitochondria at the Heart of Sepsis: Mechanisms, Metabolism, and Sex Differences.International journal of molecular sciences · 2025Review
- Reversing inflammatory diseases via trained immunity: mechanisms, challenges, and prospects.Frontiers in immunology · 2025Review
- The Role of Mitochondrial Dysfunction and Inflammatory Response in the Pathogenesis of Sepsis-Induced Myocardial Injury: A Mechanistic Study.Journal of inflammation research · 2025Review
- Regulation of hepatic Sirt1 expression and lipid metabolism through TNF receptor signaling.Frontiers in immunology · 2025Article
- Psychoneuroimmunology of Mood Disorders.Methods in molecular biology (Clifton, N.J.) · 2025Review
128 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The early initiation phase of acute inflammation is anabolic and primarily requires glycolysis with reduced mitochondrial glucose oxidation for energy, whereas the later adaptation phase is catabolic and primarily requires fatty acid oxidation for energy. We reported previously that switching from the early to the late acute inflammatory response following TLR4 stimulation depends on NAD(+) activation of deacetylase sirtuin 1 (SirT1). Here, we tested whether NAD(+) sensing by sirtuins couples metabolic polarity with the acute inflammatory response. We found in TLR4-stimulated THP-1 promonocytes that SirT1 and SirT 6 support a switch from increased glycolysis to increased fatty acid oxidation as early inflammation converts to late inflammation. Glycolysis enhancement required hypoxia-inducing factor-1α to up-regulate glucose transporter Glut1, phospho-fructose kinase, and pyruvate dehydrogenase kinase 1, which interrupted pyruvate dehydrogenase and reduced mitochondrial glucose oxidation. The shift to late acute inflammation and elevated fatty acid oxidation required peroxisome proliferator-activated receptor γ coactivators PGC-1α and β to increase external membrane CD36 and fatty acid mitochondrial transporter carnitine palmitoyl transferase 1. Metabolic coupling between early and late responses also required NAD(+) production from nicotinamide phosphoryltransferase (Nampt) and activation of SirT6 to reduce glycolysis and SirT1 to increase fatty oxidation. We confirmed similar shifts in metabolic polarity during the late immunosuppressed stage of human sepsis blood leukocytes and murine sepsis splenocytes. We conclude that NAD(+)-dependent bioenergy shifts link metabolism with the early and late stages of acute inflammation.
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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.