ArticleDiabetologia2015
Lipopolysaccharide binding protein is an adipokine involved in the resilience of the mouse adipocyte to inflammation.
Article in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
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- Autophagy: regulating the seesaw of bone-fat balance.Frontiers in cell and developmental biology · 2025Review
- Effects of altering the ratio of C16:0 and cis-9 C18:1 in rumen bypass fat on growth performance, lipid metabolism, intestinal barrier, cecal microbiota, and inflammation in fattening bulls.Journal of animal science and biotechnology · 2024Article
- Loss ofZoological research · 2024Article
- Deficiency of lipopolysaccharide binding protein facilitates adipose browning, glucose uptake and oxygen consumption in mouse embryonic fibroblasts via activating PI3K/Akt/mTOR pathway and inhibiting autophagy.Cell cycle (Georgetown, Tex.) · 2023Article
- IgM-associated gut bacteria in obesity and type 2 diabetes in C57BL/6 mice and humans.Diabetologia · 2022Article
- Specific adipose tissueMolecular therapy. Nucleic acids · 2022Article
- Lysozyme Gene Expression in 3T3-L1 Cells Sustains Expression of Adipogenic Genes and Adipocyte Differentiation.Frontiers in cell and developmental biology · 2022Article
- Local free fatty acids trigger the expression of lipopolysaccharide-binding protein in murine white adipose tissue.Bioscience of microbiota, food and health · 2022Article
- Hepatic expression of lipopolysaccharide-binding protein (Lbp) is induced by the gut microbiota through Myd88 and impairs glucose tolerance in mice independent of obesity.Molecular metabolism · 2020Article
- Postprandial Endotoxin Transporters LBP and sCD14 Differ in Obese vs. Overweight and Normal Weight Men during Fat-Rich Meal Digestion.Nutrients · 2020Article
- The gut microbiota modulates both browning of white adipose tissue and the activity of brown adipose tissue.Reviews in endocrine & metabolic disorders · 2019Review
- Serum Lipopolysaccharide-Binding Protein Levels and the Incidence of Cardiovascular Disease in a General Japanese Population: The Hisayama Study.Journal of the American Heart Association · 2019Article
- Predictors of Obesity among Gut Microbiota Biomarkers in African American Men with and without Diabetes.Microorganisms · 2019Article
- Clinical factors associated with bacterial translocation in Japanese patients with type 2 diabetes: A retrospective study.PloS one · 2019Article
- H3K36 trimethylation mediated by SETD2 regulates the fate of bone marrow mesenchymal stem cells.PLoS biology · 2018Article
- Neuroinflammation in obesity: circulating lipopolysaccharide-binding protein associates with brain structure and cognitive performance.International journal of obesity (2005) · 2017Article
- Lipopolysaccharide-binding protein is associated with arterial stiffness in patients with type 2 diabetes: a cross-sectional study.Cardiovascular diabetology · 2017Article
- Association between endotoxemia and histological features of nonalcoholic fatty liver disease.World journal of gastroenterology · 2017Article
- Lipopolysaccharide-binding protein is a negative regulator of adipose tissue browning in mice and humans.Diabetologia · 2016Article
Corrections and comments
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Authors and funding
9 authors at 7 institutions in 2 countries.
Funding
Abstract
aims/hypothesisLipopolysaccharide (LPS) binding protein (LBP) is a novel 65 kDa adipokine, linked to adipose tissue (AT) inflammation, obesity and insulin resistance, that inhibits adipocyte differentiation. Here, we investigated the molecular mechanisms behind these detrimental effects on adipogenesis through whole-genome transcriptomics and in vitro experiments.
methodsPermanent and transient knockdown (KD) and co-culture experiments were performed in 3T3-L1 and 3T3-F442A cell lines during adipocyte differentiation. Microarray gene expression was performed using Genechip Affymetrix technology and validated by real-time PCR.
resultsLBP KD of 3T3-L1 cells led to a potentiated adipocyte differentiation with a dose-response relationship; genes involved in mitochondrial biogenesis, fatty acid metabolism and peroxisome proliferator-activated receptor γ (PPAR-γ) action were dramatically upregulated in parallel to increased insulin signalling. Cells with LBP KD became refractory to proinflammatory cytokines and other inflammatory stimuli (LPS and palmitate). This phenotype, mediated through disrupted nuclear factor κB (NFκB) signalling, was reversed by a soluble factor present in a co-culture with native cells and by exogenous LBP. Double-silencing of LBP and toll-like receptor 4 (TLR4) again rendered these cells insensitive to co-culture, LBP and inflammatory factors. CONCLUSIONS/
interpretationIn summary, LBP is a proinflammatory soluble adipokine that acts as a brake for adipogenesis, strengthening the negative effects of palmitate and LPS on adipocyte differentiation.
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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.