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Review
. 2016 Sep 29;21(10):1305.
doi: 10.3390/molecules21101305.

Beneficial Effects of Tea and the Green Tea Catechin Epigallocatechin-3-gallate on Obesity

Affiliations
Review

Beneficial Effects of Tea and the Green Tea Catechin Epigallocatechin-3-gallate on Obesity

Takuji Suzuki et al. Molecules. .

Abstract

Green tea has been shown to have beneficial effects against cancer, obesity, atherosclerosis, diabetes, bacterial and viral infections, and dental caries. The catechin (-)-epigallocatechin-3-gallate (EGCG) has shown the highest biological activity among green tea catechins (GTCs) in most of the studies. While several epidemiological studies have shown the beneficial effects of tea and GTCs on obesity, some studies have failed to do this. In addition, a large number of interventional clinical studies have shown these favorable effects, and cellular and animal experiments have supported those findings, and revealed the underlying anti-obesity mechanisms. One of the mechanisms is enhanced cellular production of reactive oxygen species, which is mediated through the pro-oxidant action of EGCG, leading to the activation of adenosine monophosphate-activated protein kinase, which suppresses gene and protein expression of enzymes and transcription factors involved in adipogenesis and lipogenesis, and stimulates those involved in lipolysis. Recently, scientific evidence supporting the beneficial anti-obesity effects of green tea and GTCs has been increasing. However, future investigations are still required to clarify the reasons for the inconsistent results reported in the human studies; to achieve this, careful adjustment of confounding factors will be required.

Keywords: AMPK; adipogenesis; catechin; green tea; lipogenesis; lipolysis; obesity.

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Conflict of interest statement

All authors declare that there are no conflicts of interest in the present paper.

Figures

Figure 1
Figure 1
Chemical structures of (+)-catechin and major green tea catechins.
Figure 2
Figure 2
Effects of (−)-epigallocatechin-3-gallate (EGCG) on lipid metabolism via reactive oxygen species (ROS) and AMP-regulated protein kinase (AMPK). EGCG acts as a pro-oxidant, enhancing the generation of ROS, which activate AMPK [7,8,58,59,60]. AMPK activation suppresses adipogenesis and lipogenesis, while it increases lipolysis by regulating gene and protein expression of various enzymes and transcription factors, leading to the anti-obesity effect. Transition metal ions such as Fe(II) and Cu(II) may contribute to EGCG’s ROS-generating activity [61,62]. EGCG may also increase cellular ROS levels by decreasing the levels of antioxidant molecules, such as glutathione (GSH), and antioxidant enzymes, such as superoxide dismutase (SOD), catalase, and thioredoxin reductase (TRXR) [63,64,65]. Abca, ATP-binding cassette superfamily of transporter proteins; ACAD, acyl-CoA dehydrogenase; ACC, acetyl-CoA carboxylase; aP2, adipocyte protein 2; ATGL, adipose triglyceride lipase; GPAT, glycerol phosphate acyltransferase; LPL, lipoprotein lipase; Nrf-2, nuclear factor erythroid-2-related factor-2; PGC-1, peroxisome proliferator-activated receptor gamma coactivator-1; Pref-1, preadipocyte factor-1; SCD1, stearoyl-CoA desaturase-1; UCP, uncoupling protein.

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