ArticleNature immunology2017
Postprandial macrophage-derived IL-1β stimulates insulin, and both synergistically promote glucose disposal and inflammation.
Article in Nature immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07580079 (Anakinra for the Treatment of Recurrent Postprandial Hypoglycemia After Total Gastrectomy in a Patient With End-Stage Renal Disease), which is not on this map. Cited by 228 papers, 5 of them syntheses that pooled it.
What it found
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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
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.
Anakinra for the Treatment of Recurrent Postprandial Hypoglycemia After Total Gastrectomy in a Patient With End-Stage Renal Disease
Who cites it
228 citing papers in PubMed, 5 syntheses or guidelines pooled it, 376 citations in OpenAlex.
- Association between dietary inflammatory index and risk of chronic kidney disease and low glomerular filtration rate; a systematic review and meta-analysis of observational studies.Journal of health, population, and nutrition · 2025Pooled it
- What is the impact of ferroptosis on diabetic cardiomyopathy: a systematic review.Heart failure reviews · 2024Pooled it
- The harmful effect of ankylosing spondylitis on diabetes mellitus: new evidence from the Mendelian randomization analysis.Frontiers in endocrinology · 2024Pooled it
- The role of interleukin-1β in type 2 diabetes mellitus: A systematic review and meta-analysis.Frontiers in endocrinology · 2022Pooled it
- Type 2 Diabetes: How Much of an Autoimmune Disease?Frontiers in endocrinology · 2019Pooled it
- Acute interleukin-1β antagonism decreases systemic inflammation, increases GLP-1 release, and modulates insulin secretion in individuals with prediabetes.American journal of physiology. Endocrinology and metabolism · 2026Trial
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- Do proinflammatory cytokines play a role in clozapine-associated glycometabolism disorders?Psychopharmacology · 2021Trial
- Multiomics approaches reveal direct NF-κB p65 target genes in pancreatic islets during cytokine exposure and in type 1 diabetes.American journal of physiology. Endocrinology and metabolism · 2026Article
- Effect of Diabetic Neuropathy on Reparative Ability and Immune Response System.Molecular biotechnology · 2026Article
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- Lactate acts as a metabolic brake on inflammation by repressing NLRP3 transcription via NF-κB inhibition.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Immune context governs stage-specific responses to depleting anti-PD-1 antibody in type 1 diabetes.Cell biomaterials · 2026Article
- Acute and resolving inflammation differentially regulates beta cell function in mice via interactions between peritoneal and islet-associated macrophages.Diabetologia · 2026Article
- TREM2 sustains glucose metabolic homeostasis to drive antibacterial defense during sepsis.iScience · 2026Article
- More than Glucose Elimination: Additional Benefits of SGLT2 Inhibitors in Glomerular Diseases.Drugs · 2026Review
- Article
- [Immunometabolic disorders in type 2 diabetes mellitus mediated by NLRP3 inflammasome activation and methods of pharmacological correction thereof].Problemy endokrinologii · 2026Review
- Meta-inflammation in Hidradenitis suppurativa: from pathogenic evidence to therapeutic approaches.Frontiers in immunology · 2026Review
- Expression of IL-1β in the Left-Ventricular Myocardium of Rats with Insulin-Dependent Diabetes Mellitus and Its Combination with Arterial Hypertension.Bulletin of experimental biology and medicine · 2026Article
168 more citing papers are in PubMed but not listed here.
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Authors and funding
20 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The deleterious effect of chronic activation of the IL-1β system on type 2 diabetes and other metabolic diseases is well documented. However, a possible physiological role for IL-1β in glucose metabolism has remained unexplored. Here we found that feeding induced a physiological increase in the number of peritoneal macrophages that secreted IL-1β, in a glucose-dependent manner. Subsequently, IL-1β contributed to the postprandial stimulation of insulin secretion. Accordingly, lack of endogenous IL-1β signaling in mice during refeeding and obesity diminished the concentration of insulin in plasma. IL-1β and insulin increased the uptake of glucose into macrophages, and insulin reinforced a pro-inflammatory pattern via the insulin receptor, glucose metabolism, production of reactive oxygen species, and secretion of IL-1β mediated by the NLRP3 inflammasome. Postprandial inflammation might be limited by normalization of glycemia, since it was prevented by inhibition of the sodium-glucose cotransporter SGLT2. Our findings identify a physiological role for IL-1β and insulin in the regulation of both metabolism and immunity.
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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.