Epigallocatechin gallate attenuates diet-induced obesity in mice by decreasing energy absorption and increasing fat oxidation.
OBJECTIVE
To examine the antiobesity effect of epigallocatechin gallate (EGCG), a green tea bioactive polyphenol in a mouse model of diet-induced obesity.


METHODS
Obesity was induced in male New Zealand black mice by feeding of a high-fat diet. EGCG purified from green tea (TEAVIGO) was supplemented in the diet (0.5 and 1%). Body composition (quantitative magnetic resonance), food intake, and food digestibility were recorded over a 4-week period. Animals were killed and mRNA levels of uncoupling proteins (UCP1-3), leptin, malic enzyme (ME), stearoyl-CoA desaturase-1 (SCD1), glucokinase (GK), and pyruvate kinase (PK) were analysed in different tissues. Also investigated were acute effects of orally administered EGCG (500 mg/kg) on body temperature, activity (transponders), and energy expenditure (indirect calorimetry).


RESULTS
Dietary supplementation of EGCG resulted in a dose-dependent attenuation of body fat accumulation. Food intake was not affected but faeces energy content was slightly increased by EGCG, indicating a reduced food digestibility and thus reduced long-term energy absorption. Leptin and SCD1 gene expression in white fat was reduced but SCD1 and UCP1 expression in brown fat was not changed. In liver, gene expression of SCD1, ME, and GK was reduced and that of UCP2 increased. Acute oral administration of EGCG over 3 days had no effect on body temperature, activity, and energy expenditure, whereas respiratory quotient during night (activity phase) was decreased, supportive of a decreased lipogenesis and increased fat oxidation.


CONCLUSIONS
Dietary EGCG attenuated diet-induced body fat accretion in mice. EGCG apparently promoted fat oxidation, but its fat-reducing effect could be entirely explained by its effect in reducing diet digestibility.
Klaus
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Group of Energy Metabolism, German Institute of Human Nutrition in Potsdam, Nuthetal, Germany. klaus@mail.dife.de
Pültz
S
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Thöne-Reineke
C
C
Wolfram
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S
D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D001823:Body Composition / Q000187:drug effects; D001831:Body Temperature / Q000187:drug effects; D002153:Calorimetry, Indirect; D002352:Carrier Proteins / Q000032:analysis; D002392:Catechin / Q000031:analogs & derivatives* / Q000627:therapeutic use; D019587:Dietary Supplements; D004435:Eating / Q000187:drug effects; D005941:Glucokinase / Q000032:analysis; D007408:Intestinal Absorption / Q000187:drug effects; D007473:Ion Channels; D020738:Leptin / Q000032:analysis; D050356:Lipid Metabolism; D008291:Malate Dehydrogenase / Q000032:analysis; D008297:Male; D008565:Membrane Proteins / Q000032:analysis; D026901:Membrane Transport Proteins / Q000032:analysis; D051379:Mice; D008814:Mice, Inbred NZB; D024101:Mitochondrial Proteins / Q000032:analysis; D009765:Obesity / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D010084:Oxidation-Reduction; D011770:Pyruvate Kinase / Q000032:analysis; D013230:Stearoyl-CoA Desaturase / Q000032:analysis; D014018:Tissue Distribution; D000071256:Uncoupling Protein 1; D000071246:Uncoupling Protein 2; D000071247:Uncoupling Protein 3
D000975:Antioxidants; D002352:Carrier Proteins; D007473:Ion Channels; D020738:Leptin; D008565:Membrane Proteins; D026901:Membrane Transport Proteins; D024101:Mitochondrial Proteins; C000604371:UCP1 protein, human; C000604389:UCP2 protein, human; C000604372:Ucp1 protein, mouse; C000604390:Ucp2 protein, mouse; D000071256:Uncoupling Protein 1; D000071246:Uncoupling Protein 2; D000071247:Uncoupling Protein 3; D002392:Catechin; C045651:epigallocatechin gallate; D008291:Malate Dehydrogenase; C490333:Scd1 protein, mouse; D013230:Stearoyl-CoA Desaturase; D005941:Glucokinase; D011770:Pyruvate Kinase