Berberine inhibits 3T3-L1 adipocyte differentiation through the PPARγ pathway

Huang, Cheng; Zhang, Yuebo; Gong, Zhaohui; Sheng, Xiaoyan; Li, Zongmeng; Zhang, Wei; Qin, Ying

doi:10.1016/j.bbrc.2006.07.095

Cited by 265 publications

(176 citation statements)

References 32 publications

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“…It is reported that berberine inhibits PPARγ activity by increasing PPARγ phosphorylation [7,8] and PTEN transcrip- tion is regulated by PPARγ [31,32]. The inhibition of PPARγ by berberine was clearly illustrated by berberinemediated inhibition of 3T3-L1 adipocyte differentiation, as PPARγ is one of the most important transcription factors in adipocyte differentiation ( Figure 6A) [7,8,33,34]. In RAW264.7 cells, berberine inhibited PTEN expression induced by troglitazone, an agonist of PPARγ ( Figure 6B).…”

Section: Berberine Induces Sr-a Expression By Activating Pi3-kinase Smentioning

confidence: 87%

“…Because the serum cholesterol level is not altered in berberine-treated apoE −/− mouse, the aggravation of atherosclerosis appears to be related to the effect of berberine on SR-A expression in macrophages ( Figure 4). As berberine targets multiple types of cells, such as hepatocytes, adipocytes, muscle cells and macrophages ( Figure 2 and Figure 4) [5][6][7][8], the animal study in apoE −/− mouse is essential for understanding its potential effect in human atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

“…In 3T3-L1 adipocytes and L6 myotubes, berberine activates AMP-activated protein kinase and induces GLUT4 translocation [7]. During 3T3-L1 adipocyte differentiation induction, berberine reduces the lipid accumulation in 3T3-L1 cells by inactivating PPARγ [7,8]. These beneficial metabolic effects of berberine and its history as a non-prescription drug in China suggest that berberine has the potential to be a drug for treating hyperlipidemia, hyperglycemia and obesity.…”

Section: Introductionmentioning

confidence: 99%

“…Besides hypercholesterolemia, other factors such as LDL oxidation and increased scavenger receptors can also disrupt the cholesterol homeostasis in macrophage, induce foam cell formation and cause atherosclerosis. As berberine targets multiple types of cells such as hepatocytes, adipocytes and muscle cells [5][6][7][8], it is important to ascertain whether berberine has any effect on monocytes/macrophages, especially on foam cell formation. In order to evaluate the potential of berberine as a cholesterol-controlling drug for preventing atherosclerosis, its effect on atherosclerosis development needs to be more carefully investigated.…”

Section: Introductionmentioning

confidence: 99%

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Berberine promotes the development of atherosclerosis and foam cell formation by inducing scavenger receptor A expression in macrophage

Yao

Zheng

et al. 2009

Cell Res

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Section: Berberine Induces Sr-a Expression By Activating Pi3-kinase Smentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Berberine promotes the development of atherosclerosis and foam cell formation by inducing scavenger receptor A expression in macrophage

Yao

Zheng

et al. 2009

Cell Res

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“…Quantitative real-time PCR. Real-time PCR methods and primers were used as described (16). Total RNA was extracted with a spin column (Qiagen, Hilden, Germany) and treated with DNase I to avoid genomic DNA contamination.…”

Section: Methodsmentioning

confidence: 99%

Lecithin promotes adipocyte differentiation and hepatic lipid accumulation

Zhang

Huang²,

Sheng³

et al. 2009

Int J Mol Med

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Abstract.Lecithin is an essential biological component and widely used as a nutritional supplement for protecting cells from oxidation, increase fat burning and preventing cardiovascular disease. Lecithin contains fatty acids identified as the peroxisome proliferator-activated receptor (PPAR) agonists. However, the role of lecithin in adipogenesis and lipogenesis remains elusive. 3T3-L1 cells and mouse primary preadipocytes were used to characterize the properties of lecithin related to adipogenesis and lipogenesis. We found that lecithin promoted adipocyte differentiation and differentiation-specific gene expression, and increased triglycerides and free fatty acid levels in the adipocytes. These effects are independent of the clonal expansion of 3T3-L1 cells and the upstream PPARÁ regulator, CCAAT-enhancer-binding protein ß. Furthermore, lecithin induced lipid accumulation in human hepatoma HepG2 cells. Our data suggest that lecithin is involved in adipogenesis, lipogenesis and hepatic lipid accumulation and it is implicated in obesity and hepatic steatosis.

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Berberine acts as a natural inhibitor of Wnt/β‐catenin signaling—Identification of more active 13‐arylalkyl derivatives

et al. 2013

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Aberrant activation of the canonical Wnt/β-catenin signaling pathway has been reported for numerous tumors of different origins. In most cases, mutations in components of the Wnt signaling pathway or in β-catenin itself were detected which ultimately induce a genetic program that promotes cell proliferation and attenuates apoptosis. Thus, targeting of Wnt/β-catenin signaling is of specific therapeutic interest. Herein, we investigated the plant-derived isoquinoline alkaloid berberine, which has been reported to have anticancer activity, and synthetic 13-arylalkyl derivatives thereof for their effects on Wnt/β-catenin signaling. Berberine did not show major effects on viability of HEK-293 embryonic kidney and HCT116 colon carcinoma cells and was not toxic in concentrations up to 20 µM. Berberine inhibited β-catenin transcriptional activity and attenuated anchorage-independent growth. As a result of berberine treatment, cellular levels of active β-catenin were reduced concomitant with an increase in the expression of E-cadherin. However, in unstimulated cells, the effects on β-catenin levels were low. A screen of synthetic 13-arylalkyl berberine derivatives identified compounds exhibiting activities superior to those of the naturally occurring parent substance with more than 100-fold lower EC50 values for Wnt-repression. Thus, berberine and its synthetic derivatives represent potential therapeutic agents to inhibit Wnt/β-catenin signaling in tumorigenesis.

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Berberine inhibits 3T3-L1 adipocyte differentiation through the PPARγ pathway

Cited by 265 publications

References 32 publications

Berberine promotes the development of atherosclerosis and foam cell formation by inducing scavenger receptor A expression in macrophage

Berberine promotes the development of atherosclerosis and foam cell formation by inducing scavenger receptor A expression in macrophage

Lecithin promotes adipocyte differentiation and hepatic lipid accumulation

Berberine acts as a natural inhibitor of Wnt/β‐catenin signaling—Identification of more active 13‐arylalkyl derivatives

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