Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/319306
Type: Artigo de periódico
Title: Chronic Activation Of γ2 Ampk Induces Obesity And Reduces β Cell Function
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 γ2 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. © 2016 The Authors.
Editor: Cell Press
Citation: Cell Metabolism. Cell Press, v. 23, p. 821 - 836, 2016.
Rights: fechado
Identifier DOI: 10.1016/j.cmet.2016.04.003
Address: https://www.scopus.com/inward/record.uri?eid=2-s2.0-84964600616&partnerID=40&md5=c37bb0cf5a9c8795574ae3b78063ba3e
Date Issue: 2016
Appears in Collections:Unicamp - Artigos e Outros Documentos

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