title: Vascular and metabolic actions of the green tea polyphenol epigallocatechin gallate.
abstract: Epidemiological studies demonstrate robust correlations between green tea consumption and reduced risk of type 2 diabetes and its cardiovascular complications. However, underlying molecular, cellular, and physiological mechanisms remain incompletely understood. Health promoting actions of green tea are often attributed to epigallocatechin gallate (EGCG), the most abundant polyphenol in green tea. Insulin resistance and endothelial dysfunction play key roles in the pathogenesis of type 2 diabetes and its cardiovascular complications. Metabolic insulin resistance results from impaired insulin-mediated glucose disposal in skeletal muscle and adipose tissue, and blunted insulin-mediated suppression of hepatic glucose output that is often associated with endothelial/ vascular dysfunction. This endothelial dysfunction is itself caused, in part, by impaired insulin signaling in vascular endothelium resulting in reduced insulin-stimulated production of NO in arteries, and arterioles that regulate nutritive capillaries. In this review, we discuss the considerable body of literature supporting insulin-mimetic actions of EGCG that oppose endothelial dysfunction and ameliorate metabolic insulin resistance in skeletal muscle and liver. We conclude that EGCG is a promising therapeutic to combat cardiovascular complications associated with the metabolic diseases characterized by reciprocal relationships between insulin resistance and endothelial dysfunction that include obesity, metabolic syndrome and type 2 diabetes. There is a strong rationale for well-powered randomized placebo controlled intervention trials to be carried out in insulin resistant and diabetic populations.
authors.forename: Michelle A
authors.initials: MA
authors.lastname: Keske
authors.forename: Huei L H
authors.initials: HL
authors.lastname: Ng
authors.forename: Dino
authors.initials: D
authors.lastname: Premilovac
authors.forename: Stephen
authors.initials: S
authors.lastname: Rattigan
authors.forename: Jeong-A
authors.initials: JA
authors.lastname: Kim
authors.forename: Kashif
authors.initials: K
authors.lastname: Munir
authors.forename: Peixin
authors.initials: P
authors.lastname: Yang
authors.affiliation: Menzies Research Institute Tasmania, University of Tasmania, Hobart, Tasmania, 7000, Australia. Michelle.Keske@utas.edu.au.
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Quon
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D002318:Cardiovascular Diseases / Q000517:prevention & control*; D002392:Catechin / Q000031:analogs & derivatives* / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use; D002986:Clinical Trials as Topic; D003924:Diabetes Mellitus, Type 2 / Q000517:prevention & control*; D006801:Humans; D007333:Insulin Resistance; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D013662:Tea / Q000737:chemistry* / Q000378:metabolism
chemical_list: D013662:Tea; D009569:Nitric Oxide; D002392:Catechin; C045651:epigallocatechin gallate