ArticleDiabetologia2006
Liver X receptor agonists ameliorate TNFalpha-induced insulin resistance in murine brown adipocytes by downregulating protein tyrosine phosphatase-1B gene expression.
Article in Diabetologia, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 44 citations in OpenAlex.
- Human miR-1 Stimulates Metabolic and Thermogenic-Related Genes in Adipocytes.International journal of molecular sciences · 2024Article
- Caffeine ameliorates the metabolic syndrome in diet-induced obese mice through regulating the gut microbiota and serum metabolism.Diabetology & metabolic syndrome · 2023Article
- Metabolic Regulation of Adipose Tissue Macrophage Function in Obesity and Diabetes.Antioxidants & redox signaling · 2018Review
- Article
- Liver X receptor agonist treatment attenuates cardiac dysfunction in type 2 diabetic db/db mice.Cardiovascular diabetology · 2014Article
- Adipokines and hepatic insulin resistance.Journal of diabetes research · 2013Review
- Article
- Liver X receptors and fat cell metabolism.International journal of obesity (2005) · 2012Review
- Transcriptional integration of metabolism by the nuclear sterol-activated receptors LXR and FXR.Nature reviews. Molecular cell biology · 2012Review
- Article
- Quercetin is equally or more effective than resveratrol in attenuating tumor necrosis factor-{alpha}-mediated inflammation and insulin resistance in primary human adipocytes.The American journal of clinical nutrition · 2010Article
- Dual role of interleukin-6 in regulating insulin sensitivity in murine skeletal muscle.Diabetes · 2008Article
- Liver X Receptor: Crosstalk Node for the Signaling of Lipid Metabolism, Carbohydrate Metabolism, and Innate Immunity.Current signal transduction therapy · 2008Article
- Liver X receptors as therapeutic targets in metabolism and atherosclerosis.Current atherosclerosis reports · 2008Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisThe nuclear receptors, including nuclear receptor subfamily 1, group H, member 3 (NR1HR, also known as liver X receptor [LXR]), are sensors of cholesterol metabolism and lipid biosynthesis that have recently been proposed as insulin sensitisers. TNFalpha has been described as a link between obesity and the development of insulin resistance, an important contributor to the pathogenesis of type 2 diabetes. Therefore, we decided to investigate the ability of NR1HR agonists to ameliorate TNFalpha-induced insulin resistance in brown adipocytes.
methodsPrimary brown adipocytes from rat fetuses, and from wild-type neonate mice and neonate mice deficient in the gene encoding protein tyrosine phosphatase-1B (Ptpn1, also known as Ptp1b) were cultured in the absence or presence of TNFalpha and different nuclear receptor agonists. Among them, the unrelated NR1HR ligands T0901317, GW3965 and (22R)-hydroxycholesterol were tested. After insulin stimulation, glucose uptake and solute carrier family 2 (facilitated glucose transporter), member 4 (SLC2A4, formerly known as GLUT4) translocation were measured. Next the insulin signalling cascade was determined by submitting cells to lysis, immunoprecipitation and immunoblotting.
resultsNR1HR agonists ameliorate TNFalpha-induced insulin resistance restoring completely insulin-stimulated glucose uptake and SLC2A4 translocation to plasma membrane. This effect is parallel to the recovery of the insulin cascade insulin receptor/IRS-2/phosphatidylinositol 3-kinase/protein kinase B, and could be due to the fact that T0901317 prevents the increase of PTPN1 production and phosphatase activity produced by TNFalpha. In this regard, Ptpn1-deficient brown adipocytes showed protection against insulin resistance by TNFalpha. Moreover, we observed that T0901317 produced in itself a significant increase over basal glucose uptake consistent with an increase of SLC2A4 protein content in plasma membrane, attributable to the activation of protein kinase zeta and/or the increase of Slc2a4 expression. CONCLUSIONS/
interpretationNuclear receptors NR1HR are interesting potential targets for drug treatment of insulin resistance.
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