Proposed mechanisms of (−)-epigallocatechin-3-gallate for anti-obesity

Moon, Hee Sun; Lee, Hong Gu; Choi, Yun Jaie; Kim, Tae Gyu; Cho, Chong Su

doi:10.1016/j.cbi.2007.02.008

Cited by 138 publications

(80 citation statements)

References 84 publications

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“…Agents that act via peripheral satiety peptide systems, alter the various hypothalamic neuropeptides' CNS levels, or alter the key CNS appetite monoamine neurotransmitters' levels may be suitable candidates for drugs that will suppress appetite [74,75]. Green tea and its constituents (catechins, such as epigallo catechin (EGC) and epigallo catechin gallate (EGCG), have received tremendous attention [76,77], as several lines of evidence suggest EGCG to stimulate thermogenesis through inhibition of the catechol-O-methyltransferase enzyme involved in degradation of norepinephrine [43,57,73,78,79].…”

Section: Monoamine Neurotransmittersmentioning

confidence: 99%

Review Article: Herbal Approach for Obesity Management

Chandrasekaran¹,

Vijayalakshmi²,

Prakash³

et al. 2012

AJPS

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Obesity, a complex interplay between environmental and genetic factors and is associated with significant morbidity and mortality. Usage of herbs for the management of obesity in the recent times is attracting attention. A web and manual based literature survey was conducted to assess the amount of information available on the herbal products for weight management. Traditional literature, PubMed, Scopus, Google scholar databases were screened up to February 2012. The search words were "obesity", "herbal medicine/products/extracts", "medicinal plants", "traditional medicine", "Ayurvedic medicine" without narrowing/limiting searching words or elements. Publications only with abstracts/full articles and books were reviewed in the search. Based on the available literature, for many of the herbal and weight loss products, there is little published information and there have been no clinical trials or the level of evidence is limited. Our literature survey also indicated that these herbal products fall under an acceptable level of evidence or with no scientific background at all, or they have a scientific rational but not to an acceptance level. Attempts were made in the review to define the features of possible herbal weight loss product. An ideal herbal anti obesity product should reduce the weight by 10% over placebo of treatment by showing an evidence of improvement of bio markers like blood pressure, lipids and glycemia without any side effects.

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Section: Monoamine Neurotransmittersmentioning

confidence: 99%

Review Article: Herbal Approach for Obesity Management

Chandrasekaran¹,

Vijayalakshmi²,

Prakash³

et al. 2012

AJPS

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“…1a), the most abundant polyphenolic extract from green tea, has been under extensive investigation after emerging evidence suggested that it may improve glucose metabolism, lipid metabolism and endothelial function and reduce the effects of arthritis, neurodegenerative diseases, hypertension, coronary heart disease, obesity, inflammation, cancer and insulin resistance. [15][16][17][18][19][20][21][22][23][24] Furthermore, this multifunctional polyphenol drastically reduces cognitive impairment and amyloid deposition in Alzheimer's transgenic mice. [25][26][27] Biochemical studies indicate that the neuroprotective action of EGCG results from its ability to inhibit protein aggregation, suppress/ enhance amyloidogenic/non-amyloidogenic proteolytic processes, scavenge free radicals, chelate iron and co-modulate various other cellular pathways.…”

Section: Introductionmentioning

confidence: 99%

(−)-Epigallocatechin-3-Gallate (EGCG) Maintains κ-Casein in Its Pre-Fibrillar State without Redirecting Its Aggregation Pathway

Hudson

Ecroyd

Dehle

et al. 2009

Journal of Molecular Biology

133

120

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The polyphenol (-)-epigallocatechin-3-gallate (EGCG) has recently attracted much research interest in the field of protein-misfolding diseases because of its potent anti-amyloid activity against amyloid-beta, alphasynuclein and huntingtin, the amyloid-fibril-forming proteins involved in Alzheimer's, Parkinson's and Huntington's diseases, respectively. EGCG redirects the aggregation of these polypeptides to a disordered offfolding pathway that results in the formation of non-toxic amorphous aggregates. whether this anti-fibril activity is specific to these disease-related target proteins or ismore generic remains to be established. In addition, the mechanism by which EGCG exerts its effects, as with all anti-amyloidogenic polyphenols, remains unclear. To address these aspects, we have investigated the ability of EGCG to inhibit amyloidogenesis of the generic model fibril-forming protein RCMkappa-CN (reduced and carboxymethylated kappa-casein) and thereby protect pheochromocytoma-12 cells from RCMkappa-CN amyloid-induced toxicity. We found that EGCG potently inhibits in vitro fibril formation byRCMkappa-CN [the IC50 for 50 uM RCMkappa-CN is 1 uM]. Biophysical studies reveal that EGCG prevents RCMkappa-CN fibril formation by stabilising RCMkappa-CN in its nativelike state rather than by redirecting its aggregation to the disordered, amorphous aggregation pathway. Thus, while it appears that EGCG is a generic inhibitor of amyloid-fibril formation, the mechanism by which it achieves this inhibition is specific to the target fibril-forming polypeptide. It is proposed that EGCG is directed to the amyloidogenic sheet-turn-sheet motif of monomeric RCMkappa-CN with high affinity by strong non-specific hydrophobic associations. Additional non-covalent pi-pi stacking interactions between the polyphenolic and aromatic residues common to the amyloidogenic sequence are also implicated. The polyphenol (−)-epigallocatechin-3-gallate (EGCG) has recently attracted much research interest in the field of protein-misfolding diseases because of its potent anti-amyloid activity against amyloid-β, α-synuclein and huntingtin, the amyloid-fibril-forming proteins involved in Alzheimer's, Parkinson's and Huntington's diseases, respectively. EGCG redirects the aggregation of these polypeptides to a disordered off-folding pathway that results in the formation of non-toxic amorphous aggregates. Whether this anti-fibril activity is specific to these disease-related target proteins or is more generic remains to be established. In addition, the mechanism by which EGCG exerts its effects, as with all anti-amyloidogenic polyphenols, remains unclear. To address these aspects, we have investigated the ability of EGCG to inhibit amyloidogenesis of the generic model fibril-forming protein RCMκ-CN (reduced and carboxymethylated κ-casein) and thereby protect pheochromocytoma-12 cells from RCMκ-CN amyloid-induced toxicity. We found that EGCG potently inhibits in vitro fibril formation by RCMκ-CN [the IC 50 for 50 μM RCMκ-CN is 13 ± 1 μM]. Biophys...

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“…Wedick et al (2012) proved that a consumption of anthocyanin-rich foods, particularly blueberries and apples/pears was associated with a lower risk of type 2 diabetes in men and women. The antiobesity effect of EGCG, is supported by in vivo data, which have shown that EGCG decreased food uptake, lipid absorption, blood lipids and leptin levels, also stimulating energy expenditure, fat oxidation, high density lipoprotein levels, and fecal lipid excretion (Moon et al 2007). Green tea catechins have a protective effect on weight gain (Brown et al 2011).…”

Section: Reply From D Margina and M Iliementioning

confidence: 88%