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gallate/затлъстяване

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Страница 1 от 258 резултата

N-Oleoyl-Phosphatidyl-Ethanolamine and Epigallo Catechin-3-Gallate Mitigate Oxidative Stress in Overweight and Class I Obese People on a Low-Calorie Diet.

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Oxidative stress and lipid peroxidation are considered key factors linking obesity with its associated complications. Epigallo catechin-3-gallate (EGCG) and oleoylethanolamide, together with its phospholipid precursor N-oleoyl-phosphatidylethanolamine (NOPE), are nutritional compounds that

Dietary supplementation with epigallocatechin gallate elevates levels of circulating adiponectin in non-obese type-2 diabetic Goto-Kakizaki rats.

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Epigallocatechin gallate (EGCG) reportedly enhances plasma adiponectin levels in models of insulin resistance and obesity. In this study, we found that EGCG increases plasma adiponectin levels and decreases plasma triacylglycerol levels in non-obese diabetic Goto-Kakizaki rats with insulin secretory

Physiological effects of caffeine, epigallocatechin-3-gallate, and exercise in overweight and obese women.

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The aim of this study was to evaluate the combined effects of a 10-week exercise program with ingestion of caffeine and epigallocatechin-3-gallate (EGCG) on body composition, cardiovascular fitness, and strength in overweight and obese women. In a double-blind, placebo-controlled approach,

RNA-seq analysis of diet-driven obesity and anti-obesity effects of quercetin glucoside or epigallocatechin gallate in Drosophila adults.

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High-fat diet (HFD) feeding stimulates fat accumulation in mammals and Drosophila. In the present study, we examined whether simultaneous feeding of familiar anti-obesity drugs, quercetin glycosides (QG) and epigallocatechin gallate (EGCG), to Drosophila has the same suppressive effect

Green tea (-)-epigallocatechin-3-gallate reduces body weight with regulation of multiple genes expression in adipose tissue of diet-induced obese mice.

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OBJECTIVE The aim of this study was to investigate the antiobesity effect of (-)-epigallocatechin-3-gallate (EGCG) in diet-induced obese mice. METHODS Male C57BL/6J mice were fed on a high-fat diet for 8 weeks to induce obesity. Subsequently they were divided into 3 groups and were maintained on a

Inhibition of microsomal cortisol production by (-)-epigallocatechin-3-gallate through a redox shift in the endoplasmic reticulum--a potential new target for treating obesity-related diseases.

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Conversion of cortisone to cortisol by 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1) in the endoplasmic reticulum (ER) of the target cells is a major determinant of glucocorticoid action, and plays an important role in the development of obesity-related diseases. Inhibition of 11βHSD1 activity

Epigallocatechin Gallate as an anti-obesity therapeutic compound: an in silico approach for structure-based drug designing.

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Epigallocatechin gallate is a polyphenol of tea plants. Other than tea its trace amounts are found in apple skin, onions and plums. It has anti-adipogenic and anti-oxidant potential. It was investigated that epigallocatechin gallate stopped the adipogenic differentiation of mice mesenchymal stem

(-)-Epigallocatechin-3-gallate inhibits pancreatic lipase and reduces body weight gain in high fat-fed obese mice.

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Tea (Camellia sinensis, Theaceae) has been shown to have obesity preventive effects in laboratory studies. We hypothesized that dietary epigallocatechin-3-gallate (EGCG) could reverse metabolic syndrome in high fat-fed obese C57bl/6J mice, and that these effects were related to inhibition of

TEAVIGO (epigallocatechin gallate) supplementation prevents obesity in rodents by reducing adipose tissue mass.

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BACKGROUND This study investigated the antiobesity effects of TEAVIGO, a product providing the most abundant green tea catechin, epigallocatechin gallate (EGCG), in a pure form. Two models of diet-induced obesity and an in vitro adipocyte differentiation assay were employed. METHODS Prevention and

Epigallocatechin-3-gallate and postprandial fat oxidation in overweight/obese male volunteers: a pilot study.

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OBJECTIVE Drinking green tea is associated with many health benefits, including increased fat oxidation. We tested the hypothesis that epigallocatechin-3-gallate (EGCG), the main green tea catechin, increases fat oxidation in obese men. METHODS Ten healthy overweight/obese males (body mass index

Impact of green tea epigallocatechin-3-gallate on HIF1-α and mTORC2 expression in obese women: anti-cancer and anti-obesity effects?

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Introduction: epigallocatechin-3-gallate (EGCG) is the most abundant catechin contained in green tea (Camellia sinensis) and has been associated with anti-obesity and anti-cancer effects, but the exact molecular mechanisms remain elusive. In this context, this study was designed to improve the

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

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Green tea catechins (GTCs) are polyphenolic flavonoids formerly called vitamin P. GTCs, especially (-)-epigallocatechin-3-gallate (EGCG), lower the incidence of cancers, collagen-induced arthritis, oxidative stress-induced neurodegenerative diseases, and streptozotocin-induced diabetes. Also,

Epigallocatechin-3-gallate protects against the exacerbation of allergic eosinophilic inflammation associated with obesity in mice.

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Obesity is linked to worse asthma symptoms. Epigallocatechin-3-gallate (EGCG) reduces airway inflammation, but no study investigated the effects of EGCG on obesity-associated asthma. We aimed here to evaluate the effects of EGCG on allergen-induced airway inflammation in high-fat diet-fed mice. Male

Gallocatechin Gallate-Containing Fermented Green Tea Extract Ameliorates Obesity and Hypertriglyceridemia Through the Modulation of Lipid Metabolism in Adipocytes and Myocytes.

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Green tea is reported to exert beneficial effects on metabolic disorders through the regulation of lipid metabolism. On the contrary, fermented food products have been introduced to improve human health by modulating immune response and energy metabolism. To maximize health benefit, we applied

Epigallocatechin gallate delays the onset of type 1 diabetes in spontaneous non-obese diabetic mice.

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Type 1 diabetes (T1D) results from the autoimmune-mediated destruction of pancreatic β-cells, leading to deficiency of insulin production. Successful islet transplantation can normalise hyperglycaemia in T1D patients; however, the limited availability of the islets, loss of islet cell mass through
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