EGCG / green tea and your skin
Skin/wound repair, antioxidant activity, fibrosis, anti-ageing, cellulite
The green tea extract EGCG (epigallocatechin gallate) is the most important active molecule in green tea and responsible for most of its beneficial effects. EGCG is well researched for it's antioxidant, lipolytic, skin repair, anti-fibrotic and overall anti-ageing action.
Green tea / EGCG cream
For those reasons, EGCG is of great importance as active ingredient in anti-ageing, anti-cellulite, leg wellness, skin firming and under-eye creams [the Celluence® creams are the only cellulite creams in the world with high concentrations of 95%+ pure EGCG, plus 39x other natural anti-cellulite actives].
10/ ways the green tea extract EGCG...
...helps heal skin and wounds and fights skin ageing, fat accumulation and cellulite
10/ A polyphenolic extract from green tea leaves activates fat browning in high-fat-diet-induced obese mice
Fat browning has emerged as an attractive target for the treatment of obesity and related metabolic disorders. Its activation leads to increased energy expenditure and reduced adiposity, thus contributing to a better energy homeostasis. Green tea extracts (GTEs) were shown to attenuate obesity and low-grade inflammation and to induce the lipolytic pathway in the white adipose tissue (WAT) of mice fed a high-fat diet. The aim of the present study was to determine whether the antiobesity effect of an extract from green tea leaves was associated with the activation of browning in the WAT and/or the inhibition of whitening in the brown adipose tissue (BAT) in HF-diet induced obese mice. Mice were fed a control diet or an HF diet supplemented with or without 0.5% polyphenolic GTE for 8 weeks. GTE supplementation significantly reduced HF-induced adiposity (WAT and BAT) and HF-induced inflammation in WAT. Histological analysis revealed that GTE reduced the adipocyte size in the WAT and the lipid droplet size in the BAT. Markers of browning were induced in the WAT upon GTE treatment, whereas markers of HF-induced whitening were reduced in the BAT. These results suggest that browning activation in the WAT and whitening reduction in the BAT by the GTE could participate to the improvement of metabolic and inflammatory disorders mediated by GTE upon HF diet. Our study emphasizes the importance of using GTE as a nutritional tool to activate browning and to decrease fat storage in all adipose tissues, which attenuate obesity.
9/ Phytochemicals in regulating fatty acid β-oxidation: Potential underlying mechanisms and their involvement in obesity and weight loss.
Abstract: Excessive accumulation of fat as the result of more energy intake and less energy expenditure is known as obesity. Lipids are essential components in the human body and are vital for maintaining homeostasis and physiological as well as cellular metabolism. Fatty acid synthesis and catabolism (by fatty acid oxidation) are normal part of basic fuel metabolism in animals. Fatty acids are degraded in the mitochondria by a biochemical process called β-oxidation in which two-carbon fragments are produced in each cycle. The increase in fatty acid β-oxidation is negatively correlated with body mass index. Although healthy life style, avoiding Western diet, dieting and strenuous exercise are the commonly used methods to lose weight, they are not considered a permanent solution in addition to risk attenuation of basal metabolic rate (BMR). Pharmacotherapy offers benefits of weight loss by altering the satiety and lowering absorption of fat from the food; however, its side effects may outweigh the benefits of weight loss. Alternatively, dietary phytochemicals and natural health products offer great potential as an efficient weight loss strategy by modulating lipid metabolism and/or increasing BMR and thermogenesis. Specifically, polyphenols such as citrus flavonoids, green tea epigallocatechin gallate, resveratrol, capsaicin and curcumin, have been reported to increase lipolysis and induce fatty acid β-oxidation through modulation of hormone sensitive lipase, acetyl-coA carboxylase, carnitine acyl transferase and peroxisome proliferator-activated receptor gamma coactivator-1. In this review article, we discuss selected phytochemicals in relation to their integrated functionalities and specific mechanisms for weight loss.
8/ A-type ECG and EGCG dimers inhibit 3T3-L1 differentiation by binding to cholesterol in lipid rafts.
Abstract: The present study aimed to explore the underlying mechanisms of epicatechin-3-gallate-(4β→8, 2β→O→7)-epicatechin-3-gallate (A-type ECG dimer) and epigallocatechin-3-gallate-(4β→8, 2β→O→7)-epigallocatechin-3-gallate (A-type EGCG dimer) involved in their strong inhibitory effects on 3T3-L1 preadipocytes differentiation. In the synthetic "lipid raft-like" liposome, A-type ECG and EGCG dimers incorporated into the liposome with high affinity and decreased the fluidity of the liposome. In 3T3-L1 preadipocytes, A-type ECG and EGCG dimers possibly bonded to lipid rafts cholesterol and disrupted the integrity of lipid rafts, thus exerting their notable inhibitory effects on 3T3-L1 preadipocytes differentiation by suppressing mitotic clonal expansion process and mRNA levels of PPARγ, C/EBPα and SREBP1C. A highly positive correlation between the cholesterol binding capacity of the two dimers and their inhibitory effect on 3T3-L1 preadipocytes differentiation (R2=0.9328) was observed. Molecular dynamics simulation further verified that A-type ECG and EGCG dimers could bond to cholesterol via hydrogen bonding. The results of this study suggested that the disruption of A-type ECG and EGCG dimers on membrane lipid rafts by targeting cholesterol in the lipid rafts was involved in the underlying mechanisms of their strong inhibitory effects on 3T3-L1 preadipocytes differentiation. This broadens the understanding of the molecular mechanisms of polyphenols on modulating and controlling of metabolic dysregulation, particularly adipocyte differentiation, which is a significant risk factor associated with the development of cardiovascular disease.
7/ Green tea extract EGCG combined and quercetin fights fat tissue inflammation...
...by inhibiting the action of inflammatory response genes
[Source: Quercetin and Green Tea Extract Supplementation Downregulates Genes Related to Tissue Inflammatory Responses to a 12-Week High Fat-Diet in Mice]
6/ EGCG is a great complement to the anti-inflammatory action of the steroid drug prednisolone...
...combating inflammation via multiple, complementary to glucocorticoids, pathways. Specifically, EGCG significantly inhibits ROS and IL-8 (prednisolone doesn't) and is equally effective in fibrinogen binding (conversely, EGCG does not inhibit TNF-alpha and IL-6 that respond to prednisolone).
[Source: Head-to-Head Comparison of Anti-Inflammatory Performance of Known Natural Products In Vitro]
5/ EGCG boosts brown fat thermogenesis and mitochondrial biogenesis...
...evidenced by increased temperature, fat loss, mitochondrial DNA (mtDNA) and AMPK
[Source: Effects of epigallocatechin-3-gallate on thermogenesis and mitochondrial biogenesis in brown adipose tissues of diet-induced obese mice]
4/ The combination of genistein, EGCG and resveratrol inhibits preadipocyte differentiation...
...at low dosages in an additive manner (but not synergistically). The combination reduces levels of PPAR-gamma and C/EBP-alpha the two key preadipocyte differentiation regulators. The combination also reduced FABP4 and perilipin, two PPAR-γ/C/EBP-α downstream molecules. The individual compounds had no anti-adipogenic effect at low concentrations.
[Source: Antiadipogenic Effects and Mechanisms of Combinations of Genistein, Epigallocatechin-3-Gallate, and/or Resveratrol in Preadipocytes]
3/ EGCG acts as a caloric restriction mimetic and boosts lipolysis...
...by upregulating adipocyte autophagic lipolysis, reducing adipocyte triglycerides by 25%, intracellular ATP levels by 49% and inducing AMPK phosphorylation, indicating an energy-depleted state. However, EGCG does not casue adiciyte browing.
[Source: Effects of Epigallocatechin-3-Gallate on Autophagic Lipolysis in Adipocytes]
2/ Green tea extract EGCG can benefit hayfever by suppressing the inflammatory molecules...
...immunoglobulin E (IgE), histamine, interleukin (IL)-1β, IL-4, and IL-6 and COX-2 [Source: Anti-inflammatory effect of epigallocatechin gallate in a mouse model of ovalbumin-induced allergic rhinitis]
1/ EGCG green tea extract prevents disease by protecting mitochondria...
...from oxidative stress, by helping regulate mitochondrial metabolism and biogenesis, and by modulating cell apoptosis due to mitochondrial dysfunction [Source: Dietary Polyphenols and Mitochondrial Function: Role in Health and Disease]
epigallocatechin gallate in food protects fat cells from inflammation, helps fight cellulite
- Dietary phytochemicals called polyphenols are known potent antioxidants that protect body tissues from free radical damage and consequent inflammation.
- Inflammation and oxidative damage are key components of cellulite, as well as diabetes and several other so-called civilisation diseases, such as heart disease and arthritis.
- Recent research has now looked into 28 polyphenols (such as hesperidin, resveratrol, epigallocatechin gallate and curcumin) and concluded that those polyphenols protect fat cells from both oxidative damage and inflammation, by reducing inflammatory hormones, such as IL-6.
- This practically means that orally taken polyphenols (either as foods or as supplements) can be used in the fight against fat tissue inflammation for the prevention of diabetes and cellulite.
- Polyphenols may also be used with local application in the fight against cellulite as active ingredients in an anti-cellulite cream. Naturally, the more of those polyphenols are present in the cream the better results are to be expected, due to a synergistic effect of using multiple ingredients.
- Source: Evaluation of antioxidant properties of major dietary polyphenols and their protective effect on 3T3-L1 preadipocytes and red blood cells exposed to oxidative stress
- Abstract: "Obesity has been associated with a marked risk of metabolic diseases and requires therapeutic strategies. Changes in redox status with increased oxidative stress in adipose tissue have been linked with obesity-related disorders. Thus, the biological effect of antioxidants such as polyphenols is of high interest. We aimed to measure antioxidant capacities of 28 polyphenols representative of main dietary phenolic acids, flavonoids, stilbenes and curcuminoids. Then, 14 molecules were selected for the evaluation of their effect on 3T3-L1 preadipocytes and human red blood cells exposed to oxidative stress. Analysis of reducing and free radical-scavenging capacities of compounds revealed antioxidant properties related to their structure, with higher activities for flavonoids such as quercetin and epicatechin. Their effects on preadipocytes' viability also depended on their structure, dose and time of exposure. Interestingly, most of the compounds exhibited a protective effect on preadipocytes exposed to oxidative stress, by reversing H₂O₂-induced anti-proliferative action and reactive oxygen species production. Polyphenols also exerted an anti-inflammatory effect on preadipocytes exposed to H₂O₂ by reducing IL-6 secretion. Importantly, such antioxidant and anti-inflammatory effects were observed in co-exposition (polyphenol and prooxidant during 24 h) or pretreatment (polyphenol during 24 h, then prooxidant for 24 h) conditions. Moreover, compounds protected erythrocytes from AAPH radical-induced lysis. Finally, these results led to demonstrate that antioxidant and anti-inflammatory properties of polyphenols may depend on structure, dose, time of exposure and cell conditioning with oxidative stress. Such findings should be considered for a better understanding of polyphenols' benefits in strategies aiming to prevent obesity-related diseases."
EGCG from green tea inhibits fat tissue growth...
...by decreasing levels of PPAR-gamma and fatty acid synthase in adipocytes in a concentration-dependent manner
[Source: Epigallocatechin-3-gallate inhibits adipogenesis through down-regulation of PPARγ and FAS expression mediated by PI3K-AKT signaling in 3T3-L1 cells]