Methyl cinnamate inhibits adipocyte differentiation via activation of the CaMKK2-AMPK pathway in 3T3-L1 preadipocytes.

doi:10.1021/jf203981x

Paper

Methyl cinnamate inhibits adipocyte differentiation via activation of the CaMKK2-AMPK pathway in 3T3-L1 preadipocytes.

Published Jan 24, 2012 · Yun Chen, Meng-Hwan Lee, Chih-Chieh Hsu

Journal of agricultural and food chemistry

Q1 SJR score

65

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1

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Abstract

Methyl cinnamate, an active component of Zanthoxylum armatum , is a widely used natural flavor compound with antimicrobial and tyrosinase inhibitor activities. However, the underlying bioactivity and molecular mechanisms of methyl cinnamate on adipocyte function and metabolism remain unclear. The aim of this study was to investigate the inhibitory effect of methyl cinnamate on adipogenesis in 3T3-L1 preadipocytes. Methyl cinnamate markedly suppressed triglyceride accumulation associated with down-regulation of adipogenic transcription factor expression, including sterol regulatory element binding protein-1 (SREBP-1), peroxisome proliferator-activated receptor γ (PPARγ), and CCAAT/enhancer-binding protein α (C/EBPα). Additionally, methyl cinnamate-inhibited PPARγ activity and adipocyte differentiation were partially reversed by the PPARγ agonist troglitazone. Furthermore, methyl cinnamate stimulated Ca(2+)/calmodulin-dependent protein kinase kinase 2 (CaMKK2) and phospho-AMP-activated protein kinase (AMPK) expression during adipogenesis. This study first revealed methyl cinnamate has antiadipogenic activity through mechanisms mediated, in part, by the CaMKK2-AMPK signaling pathway in 3T3-L1 cells.

In Vitro Study

Study Snapshot

Methyl cinnamate inhibits adipogenesis in 3T3-L1 preadipocytes by activating the CaMKK2-AMPK signaling pathway, potentially reducing triglyceride accumulation and promoting weight loss.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

Methyl cinnamate inhibits adipocyte differentiation via activation of the CaMKK2-AMPK pathway in 3T3-L1 preadipocytes.

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Citations

Mechanistic insights of methylcinnamate in improving oxidative stress and inflammation in acetaminophen-induced hepatotoxic mice by upregulating Nrf2 pathway.

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Isoeugenol Inhibits Adipogenesis in 3T3-L1 Preadipocytes with Impaired Mitotic Clonal Expansion

Isoeugenol, a component of clove oil, inhibits adipogenesis in 3T3-L1 cells, suggesting it as a potential therapeutic agent for obesity treatment.

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Methyl cinnamate reduces triglyceride accumulation in HepG2 cells by activating the AMPK pathway, potentially improving lipid metabolism.

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Tibetan sheep adapt to plateau environmental changes through a synergistic response of rumen microbiota, metabolites, and host genes in lipid metabolism, energy metabolism, and immune metabolism.

Interference with DGAT Gene Inhibited TAG Accumulation and Lipid Droplet Synthesis in Bovine Preadipocytes

DGAT2 plays a more important role in regulating bovine fat metabolism, potentially leading to high-quality marbled beef.

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Zanthoxylum species have therapeutic potential due to their array of phytoconstituents, including anti-cancer, antimicrobial, and hepatoprotective properties.

Ginsenoside CK Inhibits the Early Stage of Adipogenesis via the AMPK, MAPK, and AKT Signaling Pathways

Ginsenoside CK inhibits early-stage adipogenesis in 3T3-L1 cells by activating AMPK and inhibiting ERK/p38 and AKT signaling pathways.