Article
Chronic Activation of γ2 AMPK Induces Obesity and Reduces β Cell Function.
Cell metabolism - 10 May 2016
Yavari Arash, Stocker Claire J, Ghaffari Sahar, Wargent Edward T, Steeples Violetta, Czibik Gabor, Pinter Katalin, Bellahcene Mohamed, Woods Angela, Martínez de Morentin Pablo B, Cansell Céline, Lam Brian Y H, Chuster André, Petkevicius Kasparas, Nguyen-Tu Marie-Sophie, Martinez-Sanchez Aida, Pullen Timothy J, Oliver Peter L, Stockenhuber Alexander, Nguyen Chinh, Lazdam Merzaka, O'Dowd Jacqueline F, Harikumar Parvathy, Tóth Mónika, Beall Craig, Kyriakou Theodosios, Parnis Julia, Sarma Dhruv, Katritsis George, Wortmann Diana D J, Harper Andrew R, Brown Laurence A, Willows Robin, Gandra Silvia, Poncio Victor, de Oliveira Figueiredo Márcio J, Qi Nathan R, Peirson Stuart N, McCrimmon Rory J, Gereben Balázs, Tretter László, Fekete Csaba, Redwood Charles, Yeo Giles S H, Heisler Lora K, Rutter Guy A, Smith Mark A, Withers Dominic J, Carling David, Sternick Eduardo B, Arch Jonathan R S, Cawthorne Michael A, Watkins Hugh, Ashrafian Houman
Abstract excerpt
Despite significant advances in our understanding of the biology determining systemic energy homeostasis, the treatment of obesity remains a medical challenge. Activation of AMP-activated protein kinase (AMPK) has been proposed as an attractive strategy for the treatment of obesity and its complications. AMPK is a conserved, ubiquitously expressed, heterotrimeric serine/threonine kinase whose short-term...
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