ArticleThe Journal of nutrition2013
The phospholipase C inhibitor U73122 attenuates trans-10, cis-12 conjugated linoleic acid-mediated inflammatory signaling and insulin resistance in human adipocytes.
Article in The Journal of nutrition, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 21 citations in OpenAlex.
- Molecular regulation of PLCβ signaling.Methods in enzymology · 2023Review
- The Contribution of Phospholipase C in Vomiting in the Least Shrew (Cryptotis Parva) Model of Emesis.Frontiers in pharmacology · 2021Article
- TAS2R16 Activation Suppresses LPS-Induced Cytokine Expression in Human Gingival Fibroblasts.Frontiers in immunology · 2021Article
- A genome-wide association study reveals novel genomic regions and positional candidate genes for fat deposition in broiler chickens.BMC genomics · 2018Article
- Article
- Insulin-Like Growth Factor II (IGF-II) Inhibits IL-1β-Induced Cartilage Matrix Loss and Promotes Cartilage Integrity in Experimental Osteoarthritis.Journal of cellular biochemistry · 2015Article
- Low level of trans-10, cis-12 conjugated linoleic acid decreases adiposity and increases browning independent of inflammatory signaling in overweight Sv129 mice.The Journal of nutritional biochemistry · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We have demonstrated that trans-10, cis-12 conjugated linoleic acid (18:2t10,c12)-mediated delipidation of human adipocytes was dependent on increased intracellular calcium and activation of inflammatory signaling in human primary adipocytes. These data are consistent with the actions of diacylglycerol and inositol triphosphate derived from phospholipase C (PLC)-dependent cell signaling. To test the hypothesis that PLC was an upstream activator of these cellular responses to 18:2t10,c12, primary cultures of human adipocytes were pretreated with 1-[6-((17β-3-methoxyestra-1,3,5 (10)-trien-17-yl)amino)hexyl]-1H-pyrrole-2,5-dione (U73122), a universal PLC inhibitor, followed by 18:2t10,c12 treatment. U73122 attenuated 18:2t10,c12-mediated insulin resistance within 48 h and suppression of the mRNA levels of peroxisome proliferator-activated receptor (PPAR)γ, insulin-stimulated glucose transporter-4, acetyl-CoA carboxylase-1, and stearoyl-CoA desaturase-1, and the protein levels of PPARγ within 18-24 h. U73122 inhibited 18:2t10,c12-mediated induction of the inflammatory-related genes calcium/calmodulin-dependent protein kinase-β, cyclooxygenase-2, monocyte chemoattractant protein-1, interleukin (IL)-6, and IL-8, secretion of IL-6 and IL-8, and the activation of extracellular signal-related kinase, c-Jun N-terminal kinase, and c-Jun within 18-24 h. Moreover, 18:2t10,c12 increased the mRNA levels of heat shock proteins within 6-24 h and intracellular calcium concentrations within 3 min, which were inhibited by U73122. Lastly, 18:2t10,c12 increased the abundance of PLCγ1 in the plasma membrane within 3 min. Taken together, these data suggest that PLC plays an important role in 18:2t10,c12-mediated activation of intracellular calcium accumulation, inflammatory signaling, delipidation, and insulin resistance in human primary adipocytes.
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