title: Oolong, black and pu-erh tea suppresses adiposity in mice via activation of AMP-activated protein kinase.
abstract: It is well known that tea has a variety of beneficial impacts on human health, including anti-obesity effects. It is well documented that green tea and its constituent catechins suppress obesity, but the effects of other types of tea on obesity and the potential mechanisms involved are not yet fully understood. In this study, we investigated the suppression of adiposity by oolong, black and pu-erh tea and characterized the underlying molecular mechanism in vivo. We found that the consumption of oolong, black or pu-erh tea for a period of one week significantly decreased visceral fat without affecting body weight in male ICR mice. On a mechanistic level, the consumption of tea enhanced the phosphorylation of AMP-activated protein kinase (AMPK) in white adipose tissue (WAT). This was accompanied by the induction of WAT protein levels of uncoupling protein 1 and insulin-like growth factor binding protein 1. Our results indicate that oolong, black and pu-erh tea, and in particular, black tea, suppresses adiposity via phosphorylation of the key metabolic regulator AMPK and increases browning of WAT.
authors.affiliation: Department of Agrobioscience, Graduate School of Agricultural Science, Kobe University, Nada-ku, Kobe 657-8501, Japan. ashida@kobe-u.ac.jp.
authors.forename: Yoko
authors.initials: Y
authors.lastname: Yamashita
authors.forename: Liuqing
authors.initials: L
authors.lastname: Wang
authors.forename: Lihua
authors.initials: L
authors.lastname: Wang
authors.forename: Yuki
authors.initials: Y
authors.lastname: Tanaka
authors.forename: Tianshun
authors.initials: T
authors.lastname: Zhang
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Ashida
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism*; D052242:Adiponectin / Q000097:blood; D052436:Adipose Tissue, White / Q000187:drug effects / Q000378:metabolism; D050154:Adiposity / Q000187:drug effects*; D000818:Animals; D001835:Body Weight; D022762:CCAAT-Enhancer-Binding Proteins / Q000235:genetics / Q000378:metabolism; D002110:Caffeine / Q000494:pharmacology; D002392:Catechin / Q000494:pharmacology; D002784:Cholesterol / Q000097:blood; D005243:Feces / Q000737:chemistry; D018970:Insulin-Like Growth Factor Binding Protein 1 / Q000235:genetics / Q000378:metabolism; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D024101:Mitochondrial Proteins / Q000235:genetics / Q000378:metabolism; D009765:Obesity / Q000517:prevention & control; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism; D010766:Phosphorylation; D059808:Polyphenols / Q000494:pharmacology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D013662:Tea / Q000737:chemistry*; D014280:Triglycerides / Q000097:blood; D000071256:Uncoupling Protein 1
chemical_list: D052242:Adiponectin; D022762:CCAAT-Enhancer-Binding Proteins; C530718:CEBPA protein, mouse; C519663:IGFBPL-1 protein, mouse; D018970:Insulin-Like Growth Factor Binding Protein 1; D007473:Ion Channels; D024101:Mitochondrial Proteins; D047495:PPAR gamma; D059808:Polyphenols; D012333:RNA, Messenger; D013662:Tea; D014280:Triglycerides; C000604371:UCP1 protein, human; C000604372:Ucp1 protein, mouse; D000071256:Uncoupling Protein 1; D002110:Caffeine; D002392:Catechin; D002784:Cholesterol; D055372:AMP-Activated Protein Kinases