Abstract
In our previous in vitro study, we found that chlorogenic acid (CGA) inhibited adipocyte differentiation and triglyceride (TG) accumulation, but the underlying mechanism is still unclear. Accumulative genetic evidence supports that canonical Wnt signaling is a key modulator on adipogenesis. Methods. In this study, 3T3-L1 cells were induced adipogenic differentiation and then treated with CGA. We investigate the effect of CGA in inhibiting adipogenesis and evaluate its role in modulating Wnt10b (wingless integration1 10b), β-catenin, glycogen synthase kinase-3β (GSK-3β), and peroxisome proliferator-activated receptor γ (PPAR-γ) involved in the Wnt (wingless integration1)/β-catenin signaling pathway. Results. The result showed that after CGA treatment, lipid accumulation and TG level decreased significantly in 3T3-L1 cells, indicating that CGA could inhibit adipogenesis. In addition, CGA repressed the induction of adipocyte differentiation biomarkers as PPAR-γ, adipocyte protein 2 (aP2), fatty acid synthase (FAS), and lipoprotein lipase (LPL), and the secretion of GSK-3β in a dose-dependent manner upregulated the expression of β-catenin and Wnt10b both in gene and protein levels. Moreover, CGA induced phosphorylation of GSK-3β and promoted the accumulation of free cytosolic β-catenin in 3T3-L1 adipocytes. Conclusion. Overall, these findings gave us the implications that CGA inhibits adipogenesis via the canonical Wnt signaling pathway.
Highlights
Obesity is becoming a worldwide health concern for its close association with cardiovascular disease, type 2 diabetes, hypertension, metabolic syndrome, osteoarthritis, and certain types of cancer [1]
Effect of chlorogenic acid (CGA) on the Cell Viability. e impact of CGA on cell viability was determined by the absorbance of cell suspension as optical density value (OD) value by Cell Counting Kit-8 (CCK-8) assay. 3T3-L1 cells incubated for
We further investigated the effect of CGA on lipid accumulation by adding CGA (0, 50, 100, and 200 μg/mL) and lithium chloride (LiCl) of 20 mM separately to the dimethyl sulfoxide (DMSO) and MDI induction medium of cells on Day 0 of differentiation. e final concentration of DMSO was kept at 0.1% throughout the differentiation period
Summary
Obesity is becoming a worldwide health concern for its close association with cardiovascular disease, type 2 diabetes, hypertension, metabolic syndrome, osteoarthritis, and certain types of cancer [1]. According to the World Health Organization (WHO), the worldwide prevalence of obesity nearly tripled from 1975 to 2016 [2]. E development of obesity is characterized by hypertrophy (increase in size) and hyperplasia (increase in number). Hyperplasia, defined as adipogenesis, is the process by which adipocytes develop from adipose-derived stem cells to lipoblasts, into preadipocytes, and into the mature adipocytes through cell differentiation [4]. One of the extracellular signaling pathways recently known to affect adipogenesis is the Wnt/β-catenin pathway. E importance of peculiar Wnt/β-catenin signaling has directed considerable attention in the future production of therapeutic approaches in obesity [7] One of the extracellular signaling pathways recently known to affect adipogenesis is the Wnt/β-catenin pathway. e importance of peculiar Wnt/β-catenin signaling has directed considerable attention in the future production of therapeutic approaches in obesity [7]
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