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Type: Artigo
Title: Chronic Activation Of Gamma 2 Ampk Induces Obesity And Reduces Beta Cell Function
Author: Yavari
Arash; Stocker
Claire J.; Ghaffari
Sahar; Wargent
Edward T.; Steeples
Violetta; Czibik
Gabor; Pinter
Katalin; Bellahcene
Mohamed; Woods
Angela; de Morentin
Pablo B. Martinez; Cansell
Celine; Lam
Brian Y. H.; Chuster
Andre; 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; Toth
Monika; 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
Marcio J.; Qi
Nathan R.; Peirson
Stuart N.; McCrimmon
Rory J.; Gereben
Balazs; Tretter
Laszlo; 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.; Cawthome
Michael A.; Watkins
Hugh; Ashrafian
Abstract: 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 activation has multiple beneficial metabolic effects. Whether these translate into long-term benefits for obesity and its complications is unknown. Here, we observe that mice with chronic AMPK activation, resulting from mutation of the AMPK gamma 2 subunit, exhibit ghrelin signaling-dependent hyperphagia, obesity, and impaired pancreatic islet insulin secretion. Humans bearing the homologous mutation manifest a congruent phenotype. Our studies highlight that long-term AMPK activation throughout all tissues can have adverse metabolic consequences, with implications for pharmacological strategies seeking to chronically activate AMPK systemically to treat metabolic disease.
Editor: Cell Press
Rights: fechado
Identifier DOI: 10.1016/j.cmet.2016.04.003
Date Issue: 2016
Appears in Collections:Unicamp - Artigos e Outros Documentos

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