Berberine reduces the expression of adipogenic enzymes and inflammatory molecules of 3T3-L1 adipocyte

Choi, Bong Hyuk; Ahn, In Sook; Kim, Yu Hee; Park, Ji Won; Lee, So Young; Hyun, Chang K.; Sool, Myoung

doi:10.1038/emm.2006.71

Cited by 148 publications

(95 citation statements)

References 21 publications

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“…Reductions of plasma TAG by BBR were also observed in other studies in rats with diabetes and nephritis [42,43,47]. Results from several in vitro studies have demonstrated that BBR decreases TAG levels through regulating fatty acid metabolism toward the downregulation of adipogenesis [51][52][53]. BBR upregulates the phosphorylation of the AMPactivated protein kinase (AMPK), which phosphorylates and inactivates acetyl-CoA carboxylase (ACC) [51,52].…”

Section: Discussionmentioning

confidence: 61%

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Co-administration of berberine and plant stanols synergistically reduces plasma cholesterol in rats

Xiao-ming¹,

Chen

Zidichouski³

et al. 2008

Atherosclerosis

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The objective of the present study was to determine the beneficial effects and the safety of oral administration of the combination of berberine (BBR) and plant stanols (PS) on plasma lipid profiles in male Sprague-Dawley rats. Four groups of animals were fed a cornstarch-casein-sucrose-based high-cholesterol (2%, w:w) and high-fat (27.5%) diet. Three treatment groups were supplemented with either BBR (100 mg kg −1 body weight d −1 ), PS (1% in diet, w:w), or the combination of both (BBRPS). After 6 wk, animals were sacrificed and followed immediately with the collection of blood and organ samples. Lipid analysis revealed that PS lowered plasma total cholesterol (T-C) by 18% (p = 0.067) and non-HDL-cholesterol (non-HDL-C) by 29% (p = 0.013) as compared with the control, while BBR had no effect on both T-C and non-HDL-C. The combination treatment of BBRPS reduced plasma T-C by 41% (p = 0.0002) and non-HDL-C by 59% (p < 0.0001) compared to the control group. BBR reduced plasma TG levels by 31% at a marginal significance relative to the control (p = 0.054), whereas PS had no effect. BBRPS showed an additive effect of BBR and PS on plasma TAG. PS and BBRPS both decreased liver cholesterol (p = 0.0027 and 0.0002, respectively). BBR and PS, either alone or in combination, did not show any toxic effects as assessed by plasma concentration of hepatic biochemical parameters. These results demonstrate that BBR and PS, when combined, synergistically lower plasma cholesterol levels and significantly reduce liver cholesterol, without the observation of any toxic effects. Crown

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Section: Discussionmentioning

confidence: 61%

“…The inactivation of ACC results in the inhibition of fatty acid synthesis but the enhancement of fatty acid oxidation. In addition, BBR downregulates the expression of adipogenic enzymes and transcription factors [53]. These effects collectively lead to the inhibition of TAG synthesis and consequently the reduction of plasma TAG levels.…”

Section: Discussionmentioning

confidence: 99%

Co-administration of berberine and plant stanols synergistically reduces plasma cholesterol in rats

Xiao-ming¹,

Chen

Zidichouski³

et al. 2008

Atherosclerosis

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“…To answer the question whether BBR could affect the expression of proinflammatory genes in the WAT of obese animals, we first examined the adipogenic/lipogenic gene expression in the WAT of obese db/db mice. As we and others have shown (9,23,33), BBR decreased expression of most adipogenic/lipogenic genes such as aP2, peroxisome proliferator-activated receptor-␥, acetyl-CoA carboxylase, and fatty acid synthase in the WAT of obese db/db mice (Supplemental Fig. 1; supplemental data for this article are available online at the Am J Physiol Endocrinol Metab website).…”

Section: Bbr Suppresses the Expression Of Proinflammatory Genes In Thmentioning

confidence: 99%

“…Recent studies have demonstrated that the beneficial effects of BBR on metabolic disorders including weightreducing, cholesterol-lowering, anti-lipogenic, and hypoglycemic effects (23,28,33,54) are associated with activation of AMP-activated protein kinase (AMPK) in peripheral tissues (3,7,33). Additionally, it has been also reported that BBR suppresses the expression of inflammatory molecules in several cell types (9,22,27,29,32). However, it is unclear how BBR mediates anti-inflammatory responses, especially in macrophages.…”

mentioning

confidence: 99%

Berberine suppresses proinflammatory responses through AMPK activation in macrophages

Jeong

Hsu²,

Lee³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

384

306

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Jeong HW, Hsu KC, Lee J-W, Ham M, Huh JY, Shin HJ, Kim WS, Kim JB. Berberine suppresses proinflammatory responses through AMPK activation in macrophages. Am J Physiol Endocrinol Metab 296: E955-E964, 2009. First published February 10, 2009 doi:10.1152/ajpendo.90599.2008 has been shown to improve several metabolic disorders, such as obesity, type 2 diabetes, and dyslipidemia, by stimulating AMP-activated protein kinase (AMPK). However, the effects of BBR on proinflammatory responses in macrophages are poorly understood. Here we show that BBR represses proinflammatory responses through AMPK activation in macrophages. In adipose tissue of obese db/db mice, BBR treatment significantly downregulated the expression of proinflammatory genes such as TNF-␣, IL-1␤, IL-6, monocyte chemoattractant protein-1 (MCP-1), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2). Consistently, BBR inhibited LPS-induced expression of proinflammatory genes including IL-1␤, IL-6, iNOS, MCP-1, COX-2, and matrix metalloprotease-9 in peritoneal macrophages and RAW 264.7 cells. Upon various proinflammatory signals including LPS, free fatty acids, and hydrogen peroxide, BBR suppressed the phosphorylation of MAPKs, such as p38, ERK, and JNK, and the level of reactive oxygen species in macrophages. Moreover, these inhibitory effects of BBR on proinflammatory responses were abolished by AMPK inhibition via either compound C, an AMPK inhibitor, or dominant-negative AMPK, implying that BBR would downregulate proinflammatory responses in macrophages via AMPK stimulation.mitogen-activated protein kinase; adenosine 5Ј-monophosphate-activated protein kinase; reactive oxygen species INFLAMMATION IS AN IMPORTANT RESPONSE that protects host organisms against external injuries and pathogens. Nevertheless, many recent reports (19,42,49) have suggested that obesity is tightly associated with a chronic and low-grade inflammatory state. In obese subjects, macrophage infiltration is increased into the adipose tissue, which contributes to developing insulin resistance (16,43). Inflammation is also known to trigger atherosclerosis, a coronary artery disease the hallmark of which is the formation of fatty deposits inside the artery walls (17,35,36). Thus accumulating evidence suggests that chronic inflammatory processes would constitute a crucial part in the pathogenesis of metabolic disorders including obesity, lipid dysregulation, insulin resistance, and atherosclerosis.Cellular events of inflammatory responses are associated with the redox balance and mitogen-activated protein kinase (MAPK) signaling pathways. In macrophages, lipopolysaccharide (LPS), a major component of bacterial cell walls, potently increases the levels of cellular reactive oxygen species (ROS) and MAPK phosphorylation, resulting in promoting proinflammatory responses (51). Consistently, specific inhibition of cellular ROS and MAPK suppresses inflammatory signaling, implying that the cellular regulator for ROS and MAPK activity might be a key factor for inflammatory respons...

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“…The anti-inflammatory effects of BBR have been observed in a variety of human and animal tissues, including the liver [35], adipose tissue [36], vascular endothelial cells [37], and intestine [38]. Although the detailed mechanisms remain to be determined, BBR was shown to reduce the levels of expression of genes encoding pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukins (ILs), prostaglandins (PGs), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS), in an AMPactivated protein kinase (AMPK)-dependent manner [39].…”

Section: Inflammatory Diseasesmentioning

confidence: 99%

Learning from berberine: Treating chronic diseases through multiple targets

Yao

Kong

Jiang

2014

Sci. China Life Sci.

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Although advances have been made, chemotherapy for chronic, multifactorial diseases such as cancers, Alzheimer’s disease, cardiovascular diseases and diabetes is far from satisfactory. Agents with different mechanisms of action are required. The botanic compound berberine (BBR) has been used as an over-the-counter antibacterial for diarrhea in China for many decades. Recent clinical studies have shown that BBR may be therapeutic in various types of chronic diseases. This review addresses BBR’s molecular mechanisms of action and clinical efficacy and safety in patients with type 2 diabetes, hyperlipidemia, heart diseases, cancers and inflammation. One of the advantages of BBR is its multiple-target effects in each of these diseases. The therapeutic efficacy of BBR may reflect a synergistic regulation of these targets, resulting in a comprehensive effect against these various chronic disorders. The safety of BBR may be due to its harmonious distribution into those targets. Although the single-target concept is still the principle for drug discovery and research, this review emphasizes the concept of a multiple target strategy, which may be an important approach toward the successful treatment of multifactorial chronic diseases.

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Berberine reduces the expression of adipogenic enzymes and inflammatory molecules of 3T3-L1 adipocyte

Cited by 148 publications

References 21 publications

Co-administration of berberine and plant stanols synergistically reduces plasma cholesterol in rats

Co-administration of berberine and plant stanols synergistically reduces plasma cholesterol in rats

Berberine suppresses proinflammatory responses through AMPK activation in macrophages

Learning from berberine: Treating chronic diseases through multiple targets

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