ArticleScientific reports2019
Nlrp1b1 negatively modulates obesity-induced inflammation by promoting IL-18 production.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Microglial protein kinase CK2 prevents obesity in mice potentially through NLRP3 inflammasome activation.Nature communications · 2026Article
- Intrinsically disordered regions in the NLRP family of receptors act as regulatory hubs for inflammasome condensation and activation.Frontiers in immunology · 2026Article
- Metaflammation's Role in Systemic Dysfunction in Obesity: A Comprehensive Review.International journal of molecular sciences · 2025Review
- Secreted proteins in treating metabolic dysfunction-associated steatotic liver disease: from bench towards bedside.Protein & cell · 2025Review
- Adipose tissue IL-18 production is independent of caspase-1 and caspase-11.Immunity, inflammation and disease · 2024Article
- Cell death and inflammation during obesity: "Know my methods, WAT(son)".Cell death and differentiation · 2023Review
- Serum levels of Vanin-2 increase with obesity in relation to inflammation of adipose tissue and may be a predictor of bariatric surgery outcomes.Frontiers in nutrition · 2023Article
- Effects of Vitamin D Supplementation on Adipose Tissue Inflammation and NF-κB/AMPK Activation in Obese Mice Fed a High-Fat Diet.International journal of molecular sciences · 2022Article
- An enriched environment re-establishes metabolic homeostasis by reducing obesity-induced inflammation.Disease models & mechanisms · 2022Article
- Interleukin-18 in metabolism: From mice physiology to human diseases.Frontiers in endocrinology · 2022Review
- Lipid deposition and metaflammation in diabetic kidney disease.Current opinion in pharmacology · 2020Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity-induced inflammation, triggered by lipid-mediated activation of the Nlrp3 inflammasome, results in glucose metabolism alterations and type 2 diabetes. This knowledge has been generated using animals deficient for any of the different components of this inflammasome (Caspase-1, Asc or Nlrp3) in the C57BL/6 background. Unlike C57BL/6 mice, which carry allele 2 of the Nlrp1b gene (Nlrp1b2), Balb/c mice that carry allele 1 (Nlrp1b1) are less prone to develop alterations in the glucose metabolism when fed with a high fat diet. However, the molecular bases for these metabolic differences are unknown. Here we show that the Nlrp1b1 allele down regulates the adipose tissue inflammatory response attenuating glucose intolerance and insulin resistance in obese C57BL/mice. Our results indicate that the positive effects of the Nlrp1b1 inflammasome on glucose tolerance and insulin sensitivity involve IL-18-mediated effects on lipolysis, pointing out that differential expression of allelic variants of genes coding for inflammasome components might control susceptibility or resistance to develop diabetes in obese individuals.
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