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Updated: Jun 16, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
Isorhamnetin-induced anti-adipogenesis is mediated by stabilization of beta-catenin protein
Jongsung Lee1, Jienny Lee, Eunsun Jung
1Biospectrum Life Science Institute, 101-701 SK Ventium, 522 Dangjung Dong, Gunpo City, 435-833 Gyunggi Do, Republic of Korea.
Aims:
Previous studies have shown that isorhamnetin has anti-adipogenic effects in mouse 3T3-L1 cells. This study was conducted to elucidate the inhibitory mechanisms of isorhamnetin during adipogenic differentiation of human adipose tissue-derived stem cells (hAMSCs).
Main Methods:
The effect of isorhamnetin on adipogenic differentiation of hAMSCs was quantified by Oil Red O staining and a triglyceride assay. In addition, real-time PCR and Western blot were used to determine the expression of adipogenesis-related genes.
Key Findings:
Isorhamnetin inhibited the adipocyte differentiation of hAMSCs. Additionally, when the effects of Wnt antagonists that promote adipogenesis were evaluated, isorhamnetin was found to down-regulate the mRNA levels of sFRP1 and Dkk1, but had no effect on the mRNA levels of sFRP2, sFRP3, sFRP4 and Dkk3. Isorhamnetin also inhibited the expression of Wnt receptor and co-receptor genes. Furthermore, isorhamnetin increased the protein levels of beta-catenin, an effector molecule of Wnt signaling, but had no effect on the mRNA levels of beta-catenin. The phosphorylation level of GSK 3beta was also increased by isorhamnetin. These results were confirmed by the fact that the expression of c-myc, cyclin D1 and PPARdelta, which are target genes of beta-catenin, was upregulated by isorhamnetin. Moreover, isorhamnetin reduced the mRNA expression levels of C/EBPalpha and PPARgamma, which are known to be inhibited by c-myc or by cyclin D1 and PPARdelta, respectively.
Significance:
Our results indicate that isorhamnetin inhibits the adipogenic differentiation of hAMSCs and that its mechanisms are mediated by the stabilization of beta-catenin.
Insights
Isorhamnetin inhibits human stem cell differentiation into fat cells by stabilizing beta-catenin. This natural compound
Area of Science:
- Biochemistry
- Cell Biology
- Stem Cell Research
Background:
- Isorhamnetin is known to possess anti-adipogenic properties.
- Understanding its mechanism in human cells is crucial for therapeutic development.
Purpose of the Study:
- To investigate the inhibitory mechanisms of isorhamnetin on adipogenic differentiation in human adipose tissue-derived stem cells (hAMSCs).
Main Methods:
- Quantified adipogenic differentiation using Oil Red O staining and triglyceride assays.
- Analyzed adipogenesis-related gene expression via real-time PCR and Western blot.
Main Results:
- Isorhamnetin inhibited hAMSC adipogenesis.
- Down-regulated Wnt antagonists (sFRP1, Dkk1) and Wnt receptor/co-receptor genes.
- Increased beta-catenin protein levels and GSK 3beta phosphorylation.
- Upregulated beta-catenin target genes (c-myc, cyclin D1, PPARdelta) and downregulated key adipogenic factors (C/EBPalpha, PPARgamma).
Conclusions:
- Isorhamnetin effectively inhibits adipogenic differentiation in hAMSCs.
- The mechanism involves the stabilization of beta-catenin, a key Wnt signaling effector.
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