ArticleEndocrine2007
Interleukin-18 enhances glucose uptake in 3T3-L1 adipocytes.
Article in Endocrine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Admission glucose, HbA1c levels and inflammatory cytokines in patients with acute ST-elevation myocardial infarction.Clinical proteomics · 2025Article
- 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
- Role of Inflammatory Cytokines, Growth Factors and Adipokines in Adipogenesis and Insulin Resistance.Inflammation · 2022Review
- Interleukin-18 in metabolism: From mice physiology to human diseases.Frontiers in endocrinology · 2022Review
- Cytokines and inflammation in adipogenesis: an updated review.Frontiers of medicine · 2019Review
- Review
- Endogenous interleukin 18 suppresses hyperglycemia and hyperinsulinemia during the acute phase of endotoxemia in mice.Surgical infections · 2015Article
- Interleukin-1β mediates macrophage-induced impairment of insulin signaling in human primary adipocytes.American journal of physiology. Endocrinology and metabolism · 2014Article
- The effect of chronic candesartan therapy on the metabolic profile and renal tissue cytokine levels in the obese Zucker rat.Mediators of inflammation · 2010Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In order to characterize the potential causative effects of interleukin-18 (IL-18) on insulin resistance, we measured glucose uptake in 3T3-L1 adipocytes treated with mouse recombinant IL-18. IL-18 surprisingly enhanced, rather than reduced insulin-mediated glucose uptake in adipocytes. Moreover IL-18 could counteract the glucose uptake suppression caused by tumor necrosis factor alpha in 3T3-L1 adipocytes. The mechanism dissection showed that the IL-18 upregulated phosphorylated Akt and downregulated phosphorylated P38 MAPK. These findings indicated that the elevated serum IL-18 levels in obesity and diabetes might be a compensatory response to insulin resistance.
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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.