Effects of berberine on glucose metabolism in vitro

Yin, Jun; Hu, Renming; Chen, Ming-Dao; Tang, Junling; Li, Fengying; Yang, Ying; Chen, Jialun

doi:10.1053/meta.2002.34715

Cited by 213 publications

(136 citation statements)

References 20 publications

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“…Further pharmacological studies have found that the effects of berberine include improving insulin resistance, lowering blood sugar, and correcting disorders of lipid metabolism [1][2][3][4] . Based on the effects of berberine on diabetes and the new notion that type 2 diabetes is essentially a disease of chronic inflammation, we make hypothesis if the anti-inflammation effect of Ber is related to the effect of insulin-resistance improvement.…”

Section: Discussionmentioning

confidence: 99%

“…It was initially used as a heat-clearing and detoxicating agent and an anti-inflammatory drug in clinical practice. Recently, it has been reported that activating the AMP-activated protein kinase (AMPK) pathway is the underlying mechanism for berberine improving insulin resistance, lowering blood sugar, and correcting lipid metabolism disorders [1][2][3][4] . A question will be asked if the anti-inflammatory effect of berberine is related to the effect of insulin-resistance improvement.…”

Section: Introductionmentioning

confidence: 99%

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Berberine reverses free-fatty-acid-induced insulin resistance in 3T3-L1 adipocytes through targeting IKKβ

Lu²,

Xu³

et al. 2008

WJG

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AIM:To i n v e s t i g a t e t h e e f f e c t s a n d m o l e c u l a r mechanisms of berberine on improving insulin resistance induced by free fatty acids (FFAs) in 3T3-L1 adipocytes. METHODS:The model of insulin resistance in 3T3-L1 adipocytes was established by adding palmic acid ( 0 . 5 m m o l / L ) t o t h e c u l t u re m e d i u m . B e r b e r in e treatment was performed at the same time. Glucose uptake rate was determined by the 2-deoxy-[3 H]-Dglucose method. The levels of IkB kinase beta (IKKβ) Ser 181 phosphorylation, insulin receptor substrate-1(IRS-1) Ser 307 phosphorylation, expression of IKKβ, IRS-1, nuclear transcription factor kappaB p65 (NF-κB p65), phosphatidylinositol-3-kinase p85 (PI-3K p85) and glucose transporter 4 (GLUT4) proteins were detected by Western blotting. The distribution of NF-κB p65 proteins inside the adipocytes was observed through confocal laser scanning microscopy (CLSM). RESULTS:After the intervention of palmic acid for 24 h, the insulin-stimulated glucose transport in 3T3-L1 adipocytes was inhibited by 67%. Meanwhile, the e x p re s s i o n o f I R S -1 a n d P I-3 K p 8 5 p ro t e i n wa s reduced, while the levels of IKKβ Ser 181 and IRS-1 Ser 307 phosphorylation, and nuclear translocation of NF-κB p65 protein were increased. However, the above indexes, which indicated the existence of insulin resistance, were reversed by berberine although the expression of GLUT4, IKKβ and total NF-κB p65 protein were not changed during this study. CONCLUSION:Insulin resistance induced by FFAs in 3T3-L1 adipocytes can be improved by berberine. Berberine reversed free-fatty-acid-induced insulin resistance in 3T3-L1 adipocytes through targeting IKKβ.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Berberine reverses free-fatty-acid-induced insulin resistance in 3T3-L1 adipocytes through targeting IKKβ

Lu²,

Xu³

et al. 2008

WJG

View full text Add to dashboard Cite

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“…Berberine has been used extensively in Orient to treat a variety of diseases. It is reported to be effective in lowering blood glucose and low-density lipoprotein cholesterol and inhibiting aldose reductase [20,33,34], as well as preventing SMC proliferation [21]. However, the precise mechanism involved in berberine-mediated antiproliferative effect in vascular cells has not been well addressed.…”

Section: Discussionmentioning

confidence: 99%

Berberine suppresses MEK/ERK-dependent Egr-1 signaling pathway and inhibits vascular smooth muscle cell regrowth after in vitro mechanical injury

Liang

Ting

Yin

et al. 2006

Biochemical Pharmacology

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Vascular smooth muscle cell (SMC) proliferation plays an important role in the pathogenesis of atherosclerosis and post-angioplasty restenosis. Berberine is a well-known component of the Chinese herb medicine Huanglian (Coptis chinensis), and is capable of inhibiting SMC contraction and proliferation, yet the exact mechanism is unknown. We therefore investigated the effect of berberine on SMC growth after mechanic injury in vitro. DNA synthesis and cell proliferation assay were performed to show that berberine inhibited serum-stimulated rat aortic SMC growth in a concentration-dependent manner. Mechanical injury with sterile pipette tip stimulated the regrowth of SMCs. Treatment with berberine prevented the regrowth and migration of SMCs into the denuded trauma zone. Western blot analysis showed that activation of the MEK1/2 (mitogen-activated protein kinase kinase 1/2), extracellular signal-regulated kinase (ERK), and up-regulation of early growth response gene (Egr-1), c-Fos and Cyclin D1 were observed sequentially after mechanic injury in vitro. Semi-quantitative reverse-transcription PCR assay further confirmed the increase of Egr-1, cFos, platelet-derived growth factor (PDGF) and Cyclin D1 expression in a transcriptional level. However, berberine significantly attenuated MEK/ERK activation and downstream target (Egr-1, cFos, Cyclin D1 and PDGF-A) expression after mechanic injury in vitro. Our study showed that berberine blocked injury-induced SMC regrowth by inactivation of ERK/Egr-1 signaling pathway thereby preventing early signaling induced by injury in vitro. The anti-proliferative properties of berberine may be useful in treating disorders due to inappropriate SMC growth.

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“…These works show that this plant species generates a decrease in blood glucose levels in different murine species [11][12][13][14][15][16][17][18][19]. Berberine, the active compound of this species, is also described as a glucose uptake stimulator in HepG2 cells [20]. Similarly, the root extract of B. microphylla stimulates the uptake of glucose in HepG2 cells, beginning with the tested concentration of 1.25 x 10-3 μg/μL; the root extract also exerts this same effect on resistant hepatic cells at the sameextract also exerts this same effect on resistant hepatic cells HepG2 at the same concentration and in both cases generates a dose-dependent response.…”

Section: Discussionmentioning

confidence: 99%