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Vascular and metabolic actions of the green tea polyphenol epigallocatechin gallate

Keske, Michelle A., Ng, Huei L.H., Premilovac, Dino, Rattigan, Stephen, Kim, Jeong-a, Munir, Kashif, Yang, Peixin and Quon, Michael J. 2015, Vascular and metabolic actions of the green tea polyphenol epigallocatechin gallate, Current medicinal chemistry, vol. 22, no. 1, pp. 59-69, doi: 10.2174/0929867321666141012174553.

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Title Vascular and metabolic actions of the green tea polyphenol epigallocatechin gallate
Author(s) Keske, Michelle A.ORCID iD for Keske, Michelle A. orcid.org/0000-0003-4214-7628
Ng, Huei L.H.
Premilovac, Dino
Rattigan, Stephen
Kim, Jeong-a
Munir, Kashif
Yang, Peixin
Quon, Michael J.
Journal name Current medicinal chemistry
Volume number 22
Issue number 1
Start page 59
End page 69
Total pages 11
Publisher Bentham Science Publishers
Place of publication Beijing, China
Publication date 2015
ISSN 0929-8673
1875-533X
Keyword(s) Adipose Tissue
Animals
Cardiovascular Diseases
Catechin
Clinical Trials as Topic
Diabetes Mellitus, Type 2
Humans
Insulin Resistance
Liver
Muscle, Skeletal
Nitric Oxide
Tea
Science & Technology
Life Sciences & Biomedicine
Biochemistry & Molecular Biology
Chemistry, Medicinal
Pharmacology & Pharmacy
EGCG
endothelial function
green tea
insulin action
insulin sensitivity
metabolism
muscle blood flow
type 2 diabetes
Summary 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.
Language eng
DOI 10.2174/0929867321666141012174553
Field of Research 110399 Clinical Sciences not elsewhere classified
111603 Systems Physiology
110201 Cardiology (incl Cardiovascular Diseases)
110306 Endocrinology
111103 Nutritional Physiology
0304 Medicinal And Biomolecular Chemistry
1115 Pharmacology And Pharmaceutical Sciences
Socio Economic Objective 920104 Diabetes
HERDC Research category C1.1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Grant ID NHMRC 1009962
Copyright notice ©2015, Bentham Science Publishers
Persistent URL http://hdl.handle.net/10536/DRO/DU:30092193

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