Green tea (Camellia sinensis, Theaceace) is the second most popular beverage in the world and has been extensively studied for its putative disease preventive effects. Green tea is characterized by the presence of a high concentrations of polyphenolic compounds known as catechins, with (−)-epigallocatechin-3-gallate (EGCG) being the most abundant and most well-studied. Metabolic syndrome (MetS) is a complex condition that is defined by the presence of elevated waist circumference, dysglycemia, elevated blood pressure, decrease serum high density lipoprotein-associated cholesterol, and increased serum triglycerides. Studies in both in vitro and laboratory animal models have examined the preventive effects of green tea and EGCG against the symptoms of MetS. Overall, the results of these studies have been promising and demonstrate that green tea and EGCG have preventive effects in both genetic and dietary models of obesity, insulin resistance, hypertension, and hypercholesterolemia. Various mechanisms have been proposed based on these studies and include: modulation of dietary fat absorption and metabolism, increased glucose utilization, decreased de novo lipogenesis, enhanced vascular responsiveness, and antioxidative effects. In the present review, we discuss the current state of the science with regard to laboratory studies on green tea and MetS. We attempt to critically evaluate the available data and point out areas for future research. Although there is a considerable amount of data available, questions remain in terms of the primary mechanism(s) of action, the dose-response relationships involved, and the best way to translate the results to human intervention studies.

(−)-Epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, has been shown to prevent the development of obesity in rodent models. Here, we examined the effect of EGCG on markers of fat oxidation in high fat-fed C57bl/6J mice. High fat-fed mice treated with 0.32% dietary EGCG for 16 weeks had reduced body weight gain and final body weight (19.2% and 9.4%, respectively) compared to high fat-fed controls. EGCG-treatment decreased fasting blood glucose, plasma insulin, and insulin resistance by 18.5%, 25.3%, and 33.9%, respectively. EGCG treatment also reduced markers of obesity-related fatty liver disease in high fat-fed mice. Gene expression analysis of skeletal muscle showed that EGCG increased mRNA levels of nuclear respiratory factor (nrf)1, medium chain acyl coA decarboxylase (mcad), uncoupling protein (ucp)3, and peroxisome proliferator responsive element (ppar)α by 1.4 – 1.9-fold compared to high fat-fed controls. These genes are all related to mitochondrial fatty acid oxidation. In addition, EGCG increased fecal excretion of lipids in high fat-fed mice. In summary, it appears that EGCG modulates body weight gain in high fat-fed mice both by increasing the expression of genes related fat oxidation in the skeletal muscle and by modulating fat absorption from the diet.

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 pancreatic lipase (PL). Following treatment with 0.32% EGCG for 6 weeks, a 44% decrease in body weight (BW) gain in high fat‐fed, obese mice (P < 0.01) was observed compared to controls. EGCG treatment increased fecal lipid content by 29.4% (P < 0.05) compared to high fat‐fed control, whereas in vitro, EGCG dose‐dependently inhibited PL (IC50 = 7.5 µmol/l) in a noncompetitive manner with respect to substrate concentration. (−)−Epicatechin‐3‐gallate exhibited similar inhibitory activity, whereas the nonester‐containing (−)−epigallocatechin did not. In conclusion, EGCG supplementation reduced final BW and BW gain in obese mice, and some of these effects may be due to inhibition of PL by EGCG.

Oxidative stress is known to play a key role in estrogen-induced breast cancer. This study assessed the chemopreventive activity of the naturally occurring γ-tocopherol-rich mixture of tocopherols (γ-TmT) in early stages of estrogen-induced mammary hyperplasia in ACI rats. ACI rats provide an established model of rodent mammary carcinogenesis due to their high sensitivity to estrogen. Female rats were implanted with 9 mg of 17β-estradiol (E2) in silastic tubings and fed with control or 0.3% γ-TmT diet for 1, 3, 7 and 14 days. γ-TmT increased the levels of tocopherols and their metabolites in the serum and mammary glands of the rats. Histological analysis revealed mammary hyperplasia in the E2 treated rats fed with control or γ-TmT diet. γ-TmT decreased the levels of E2-induced nitrosative and oxidative stress markers, nitrotyrosine and 8-oxo-dG, respectively, in the hyperplastic mammary tissues. 8-Isoprostane, a marker of oxidative stress in the serum, was also reduced by γ-TmT. Noticeably, γ-TmT stimulated Nrf2-dependent antioxidant response in the mammary glands of E2 treated rats, evident from the induced mRNA levels of Nrf2 and its downstream antioxidant enzymes, superoxide dismutase, catalase and glutathione peroxidase. Therefore, inhibition of nitrosative/oxidative stress through induction of antioxidant response is the primary effect of γ-TmT in early stages of E2-induced mammary hyperplasia. Due to its cytoprotective activity, γ-TmT could be a potential natural agent for the chemoprevention of estrogen-induced breast cancer.

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This study evaluated the anti-cancer activity and mechanism of action of a γ-tocopherol rich tocopherol mixture, γ-TmT, in two different animal models of estrogen-induced breast cancer. The chemopreventive effect of γ-TmT at early (6 weeks), intermediate (18 weeks) and late (31 weeks) stages of mammary tumorigenesis was determined using the ACI rat model. Female rats receiving 17β-estradiol (E2) implants were administered with different doses (0, 0.05%, 0.1%, 0.3% and 0.5%) of γ-TmT diet. Treatment with 0.3% and 0.5% γ-TmT decreased tumor volume and multiplicity. At 31 weeks, serum concentrations of E2 were significantly decreased by γ-TmT. γ-TmT preferentially induced expression of the E2 metabolizing enzyme CYP1A1, over CYP1B1 in the rat mammary tissues. Nrf2-dependent antioxidant response was stimulated by γ-TmT, as evident from enhanced expression of its downstream targets, NQO1, GCLM and HMOX1. Serum concentrations of the oxidative stress marker, 8-isoprostane, were also decreased in the γ-TmT treated groups. Treatment with γ-TmT increased expression of PPARγ and its downstream genes, PTEN and p27, while the cell proliferation marker, PCNA, was significantly reduced in γ-TmT treated mammary tumors. In an orthotopic model in which human MCF-7 breast cancer cells were injected into the mammary fat pad of immunodeficient mice, γ-TmT inhibited E2-dependent tumor growth at all the doses tested. In conclusion, γ-TmT reduced mammary tumor development, in part through decreased E2 availability and reduced oxidative stress in mammary tissues; γ-TmT could thus be an effective agent for the prevention and treatment of E2-induced breast cancer.

Obesity and metabolic syndrome are growing public health problems. We investigated the effects of decaffeinated green tea extract (GTE) and voluntary running exercise (Ex) alone or in combination against obesity and metabolic syndrome in high fat (HF) fed C57BL/6J mice. After 16 wk, GTE + Ex treatment reduced final body mass (27.1% decrease) and total visceral fat mass (36.6% decrease) compared to HF-fed mice. GTE + Ex reduced fasting blood glucose (17% decrease), plasma insulin (65% decrease), and insulin resistance (65% decrease) compared to HF-fed mice. GTE or Ex alone had less significant effects. In the skeletal muscle, the combination of Ex and GTE increased the expression of peroxisome proliferator-activated receptor-γ coactivator-1α (Ppargc1a), mitochondrial NADH dehydrogenase 5 (mt-Nd5), mitochondrial cytochrome b (mt-Cytb), and mitochondrial cytochrome c oxidase III (mt-Co3). An increase in hepatic expression of peroxisome proliferator-activated receptor-α (Ppara) and liver carnitine palmitoyl transferase-1α (Cpt1a) and a decrease in hepatic expression of stearoyl-CoA desaturase 1 (Scd1) mRNA was observed in GTE + Ex mice. GTE + Ex was more effective than either treatment alone in reducing diet-induced obesity. These effects are due in part to modulation of genes related to energy metabolism and de novo lipogenesis.

Purpose Food taboos during pregnancy and the postpartum period have been linked to increased risk of maternal and neonatal death. This paper aims to present plant-based food restrictions on Southeast Asian women during pregnancy and after giving birth and the rationale behind such cultural practices. Design/methodology/approach Google® Scholar, PubMed and Scopus search using the term food taboo, its synonyms and truncations, in combination with the terms pregnancy, postpartum and breastfeeding, and with the name of the Southeast Asian countries, was conducted from January to February 2017. Articles were included in the review if their full texts were accessible online, in English, published from 2005 to 2016 and if they contained primary data from either quantitative or qualitative method. Findings A total of 281 articles were downloaded, and 28 were included in this review. The food taboos and the reasons for avoidance were collated and grouped per their occurrence and according to the country or countries where they are practiced. In total, 14 papers generated data on food taboos during pregnancy, 16 papers on postpartum food taboos and/or 6 on breastfeeding. Research limitations/implications This review pools together relevant information about plant-based food taboos Southeast Asian women adhere to during pregnancy and after giving birth. However, data are absent for some of the Association of Southeast Asian Nations (ASEAN) countries, and there is a need for more research to get up-to-date information on the local women’s adherence to these cultural practices. Practical implication The knowledge of these practices can support stakeholders who are contributing to the reduction of maternal and under-five mortality ratios in Southeast Asia. Originality/value This is the first review paper on food taboos covering all ASEAN members and highlighting the need for cultural sensitivity to properly address maternal and child health problems in the region.