Abstract
The pandemic proportion of diabesity—a combination of obesity and diabetes—sets a worldwide health issue. Experimental and clinical studies have progressively reinforced the pioneering epidemiological observation of an inverse relationship between consumption of polyphenol-rich nutraceutical agents and mortality from cardiovascular and metabolic diseases. With chemical identification of epigallocatechin-3-gallate (EGCG) as the most abundant catechin of green tea, a number of cellular and molecular mechanisms underlying the activities of this unique catechin have been proposed. Favorable effects of EGCG have been initially attributed to its scavenging effects on free radicals, inhibition of ROS-generating mechanisms and upregulation of antioxidant enzymes. Biologic actions of EGCG are concentration-dependent and under certain conditions EGCG may exert pro-oxidant activities, including generation of free radicals. The discovery of 67-kDa laminin as potential EGCG membrane target has broaden the likelihood that EGCG may function not only because of its highly reactive nature, but also via receptor-mediated activation of multiple signaling pathways involved in cell proliferation, angiogenesis and apoptosis. Finally, by acting as epigenetic modulator of DNA methylation and chromatin remodeling, EGCG may alter gene expression and modify miRNA activities. Despite unceasing research providing detailed insights, ECGC composite activities are still not completely understood. This review summarizes the most recent evidence on molecular mechanisms by which EGCG may activate signal transduction pathways, regulate transcription factors or promote epigenetic changes that may contribute to prevent pathologic processes involved in diabesity and its cardiovascular complications.
Highlights
IntroductionThe term “diabesity” has been coined to emphasize the close relationship between obesity and Type
The term “diabesity” has been coined to emphasize the close relationship between obesity and Type2 diabetes mellitus (T2DM) [1,2,3]
Beneficial effects of tea and its catechins have been reported in obese individuals [36,87], discrepancies have emerged based on sex, age or population characteristics: for example, tea consumption was negatively associated with obesity and fasting blood glucose level in women, but not in men, in a Polish population [88], whereas no association was found between green tea consumption and the prevalence of metabolic syndrome or any of its components in a Japanese population [89]
Summary
The term “diabesity” has been coined to emphasize the close relationship between obesity and Type. ROS derived by the initial overproduction of superoxide by the mitochondrial electron-transport chain contribute to permanent alteration of cell components including proteins and lipids, and may induce post-translational modifications of histones causing chromatin remodeling and change in levels of gene expression [17] All these phenomena underlie the development and progression of micro-and macrovascular complications, and predispose to cardiovascular morbidity and mortality events [18]. While preclinical studies have reported that some vitamins and supplements can help lower markers of oxidative stress such as reduced plasma levels of lipoic acid and glutathione -consistently measured in diabetic patients with micro- and–macrovascular complications- other investigations conclude that most of these antioxidants do not accomplish any substantial benefit in humans [8,20,21,22] These disappointing results have been explained, in part, by the fact that conventional antioxidants usually neutralize reactive oxygen molecules on a one-for-one basis, while diabesity-induced overproduction of superoxide is a continuous process. Epidemiological observations reporting EGCG effects in obesity or diabetes are briefly summarized, with subsequent focus on mechanisms underlying EGCG-mediated protection in lipid alteration, glucose impairment and vascular complications
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