Effects of dietary supplementation with epigallocatechin-3-gallate on weight loss, energy homeostasis, cardiometabolic risk factors and liver function in obese women: randomised, double-blind, placebo-controlled clinical trial
What this study found
EGCG did not add benefit to the energy-restricted diet. Compared with placebo, there were no significant differences in changes in body weight, BMI, fat mass, lean mass, waist circumference, resting metabolic rate, glucose, insulin, HOMA-IR, lipids, CRP, or liver enzymes after 12 weeks. The supplement was well tolerated, and no participants withdrew because of discomfort or adverse effects; no adverse effects on liver biomarkers were seen. The active group randomized 43 participants and 39 were analyzed at follow-up, versus 40 randomized and 39 analyzed in the placebo group.
- Study & population
- Randomized, double-blind, placebo-controlled trial in obese premenopausal Caucasian women from Vitoria-Gasteiz, Spain.
- Intervention
- Epigallocatechin-3-gallate (EGCG) was given orally as green tea extract TEAVIGO TM at 300 mg/day, divided into three doses with breakfast, lunch, and dinner for 12 weeks.
- Key limitation
- The trial was relatively small, with only 39 analyzed participants in the EGCG group and 39 in placebo, which limits power to detect modest effects.
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Open PDFOriginal abstract
The aim of the present study was to examine the effects of green tea epigallocatechin-3-gallate (EGCG) on changes in body composition, energy and substrate metabolism, cardiometabolic risk factors and liver function enzymes after an energy-restricted diet intervention in obese women. In the present randomised, double-blind, placebo-controlled study, eighty-three obese (30 kg/m2>BMI < 40 kg/m2) pre-menopausal women consumed 300 mg/d of EGCG or placebo (lactose). We measured body weight and adiposity (dual-energy X-ray absorptiometry), energy expenditure and fat oxidation rates (indirect calorimetry), blood lipid levels (TAG, total cholesterol, LDL-cholesterol and HDL-cholesterol), insulin resistance, C-reactive protein and liver function markers (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, γ-glutamyltransferase, urea, bilirubin and 2-keto[1-13C]isocaproate oxidation) before and after the intervention in the EGCG and control groups. We did not find any significant difference in the changes in body weight ( − 0·3 kg, 95 % CI − 5·0, 4·3), fat mass ( − 0·7 kg, 95 % CI − 3·5, 2·1), energy (0·3 kJ/kg per d, 95 % CI − 3·1, 2·7) and fat ( − 0·1 g/min, 95 % CI − 0·03, 0·01) metabolism, homeostasis assessment model for insulin resistance (0·2, 95 % CI − 0·2, 0·7), total cholesterol ( − 0·21 mmol/l, 95 % CI − 0·55, 0·13), LDL-cholesterol ( − 0·15 mmol/l, 95 % CI − 0·50, 0·20), TAG ( − 0·14 mmol/l, 95 % CI − 0·56, 0·29) and liver function markers between the EGCG and control groups. In conclusion, the present results suggest that dietary supplementation with 300 mg/d of EGCG for 12 weeks did not enhance energy-restricted diet-induced adiposity reductions, and did not improve weight-loss-induced changes in cardiometabolic risk factors in obese Caucasian women. The intake of 300 mg/d of EGCG for 12 weeks did not cause any adverse effect on liver function biomarkers.