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The Effects of Epigallocatechin-3-Gallate on Thermogenesis and Fat Oxidation in Obese Men: A Pilot Study

Michael Boschmann, MD and Frank Thielecke, PhD

Universitary Medicine Berlin, Charité Campus Buch, Franz Volhard Center for Clinical Research, and HELIOS Clinic Berlin Buch, (M.B.), GERMANY
DSM Nutritional Products (F.T.), Basel, SWITZERLAND


Figure 1
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Fig. 1. Mechanisms by which EGCG may decrease energy intake, increase energy expenditure, and reduce adipose tissue mass and prevent or treat obesity and its associated diseases, diabetes and hypertension (adapted from [8]). Abbreviations: HDL, high density lipoprotein; LDL, low density lipoprotein; VLDL, very low density lipoprotein; IGF, insulin-like growth factor; CCK, cholecystokinin; GLUT4, glucose transporter 4; ACC, acetyl-CoA carboxylase; FAS, fatty acid synthase; GPDH, {alpha}-glycerophosphate dehydrogenase; SCD1, stearoyl-CoA desaturase 1; HSL, hormone sensitive lipase.

 

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Fig. 2. Time course of energy expenditure (EE, upper panel) and respiratory quotient (RQ, lower panel) before and after intake of a test meal with EGCG or placebo. See text for details of supplementation and meal composition. Data are given as mean ± SD

 

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Fig. 3. Targets of different drugs within the sympathetic nervous system that increase the availability of norepinephrine (NE) within the synaptic cleft (EGCG, ephedrine, amphetamine, sibutramine) or prolong NE-induced increases in lipid mobilization and oxidation (caffeine). Abbreviations: NE, norepinephrine; COMT, catechol-O-methyl transferase; ß-AR, ß-adrenoreceptor; Gs, stimulatory G-protein; PKA, protein kinase A; HSL, hormone sensitive lipase; TAG, triacylglycerol; FFA, free fatty acids; PDE, phosphodiesterase.

 





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