ArticlePharmaceutical biology2017
Caffeic acid methyl and ethyl esters exert potential antidiabetic effects on glucose and lipid metabolism in cultured murine insulin-sensitive cells through mechanisms implicating activation of AMPK.
Article in Pharmaceutical biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
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- Polyphenols as potential metabolism mechanisms regulators in liver protection and liver cancer prevention.Cell proliferation · 2023Review
- Constituents of Morus alba var. multicaulis leaf improve lipid metabolism by activating the AMPK signaling pathway in HepG2 cells.Journal of natural medicines · 2022Article
- Caffeic Acid on Metabolic Syndrome: A Review.Molecules (Basel, Switzerland) · 2021Review
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- Maca extracts regulate glucose and lipid metabolism in insulin-resistant HepG2 cells via the PI3K/AKT signalling pathway.Food science & nutrition · 2021Article
- Bioactivity-Guided Isolation of Phytochemicals fromMolecules (Basel, Switzerland) · 2021Article
- Cellular and molecular effects of Baccharis dracunculifolia D.C. and Plectranthus barbatus Andrews medicinal plant extracts on retinoid metabolism in the human hepatic stellate cell LX-2.BMC complementary and alternative medicine · 2019Article
- Fridamycin A, a Microbial Natural Product, Stimulates Glucose Uptake without Inducing Adipogenesis.Nutrients · 2019Article
- Rapid UHPLC-MS metabolite profiling and phenotypic assays reveal genotypic impacts of nitrogen supplementation in oats.Metabolomics : Official journal of the Metabolomic Society · 2019Article
- Insulin Mimetic Properties of Extracts Prepared fromMolecules (Basel, Switzerland) · 2018Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
contextCaffeic acid methyl (CAME) and ethyl (CAEE) esters stimulate glucose uptake and AMP-activated protein kinase (AMPK) in C2C12 myocytes (ATCC
objectiveEffects of CAME and CAEE were now assessed on myocyte glucose transporter GLUT4 activity and expression, on hepatic gluconeogenesis and on adipogenesis as well as major underlying signaling pathways. MATERIALS AND
methodsGLUT4 protein translocation was studied in L6 GLUT4myc cells, glucose-6-phospatase (G6Pase) in H4IIE hepatocytes and adipogenesis in 3T3-L1 adipocytes. Key modulators were measured using western immunoblot. Cells were treated for 18 h with either CAME or CAEE at various concentrations (12.5-100 μM).
resultsMyocyte glucose uptake rose from 10.1 ± 0.5 to 18.7 ± 0.8 and 21.9 ± 1.0 pmol/min/mg protein in DMSO-, CAME- and CAEE-stimulated cells, respectively, similar to insulin (17.7 ± 1.2 pmol/min/mg protein), while GLUT4myc translocation increased significantly by 1.70 ± 0.18, by 1.73 ± 0.18- and by 1.95 ± 0.30-fold (relative to DMSO), following insulin, CAME and CAEE stimulation, respectively. CAME and CAEE suppressed hepatocyte G6Pase by 62.0 ± 6.9% and 62.7 ± 6.0% with IC DISCUSSION AND
conclusionsCAME and CAEE exerted antidiabetic activities in insulin-responsive cells through insulin-independent mechanisms involving AMPK and adipogenic factors.
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