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Publication : Chronic Activation of γ2 AMPK Induces Obesity and Reduces β Cell Function.

First Author	Yavari A	Year	2016
Journal	Cell Metab	Volume	23
Issue	5	Pages	821-36
PubMed ID	27133129	Mgi Jnum	J:235379
Mgi Id	MGI:5796216	Doi	10.1016/j.cmet.2016.04.003
Citation	Yavari A, et al. (2016) Chronic Activation of gamma2 AMPK Induces Obesity and Reduces beta Cell Function. Cell Metab 23(5):821-36

abstractText

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 gamma2 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.

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Publication : Chronic Activation of γ2 AMPK Induces Obesity and Reduces β Cell Function.

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