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Food anticipatory activity on a calorie-restricted diet is independent of Sirt1

Assali, Dina R. and Hsu, Cynthia T. and Gunapala, Keith M. and Aguayo, Antonio and McBurney, Michael and Steele, Andrew D. (2018) Food anticipatory activity on a calorie-restricted diet is independent of Sirt1. PLoS ONE, 13 (6). Art. No. e0199586. ISSN 1932-6203. PMCID PMC6016907.

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[img] Postscript (S1 Fig. Testing FAA in tyrosine hydroxylase Cre deletion mutants of Sirt1) - Supplemental Material
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[img] MS Excel (S1 Dataset. Behavior, body weight, and food intake for each mouse line used in this study) - Supplemental Material
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A number of studies have demonstrated that the Sirtuin family member, Sirt1, is a key integrator of growth, metabolism, and lifespan. Sirt1 directly interacts with and deacetylates key regulators of the circadian clock, positioning it to be an important link between feeding and circadian rhythms. In fact, one study suggests that Sirt1 is necessary for behavioral anticipation of limited daily food availability, a circadian process termed food anticipatory activity (FAA). In their study, mice overexpressing Sirt1 had enhanced FAA, while mice lacking Sirt1 had little to no FAA. Based on the supposition that Sirt1 was indeed required for FAA, we sought to use Sirt1 deletion to map the neural circuitry responsible for FAA. We began by inactivating Sirt1 using the cell-type specific Cre-driver lines proopiomelanocortin, but after observing no effect on body weight loss or FAA we then moved on to more broadly neuronal Cre drivers Ca2+/calmodulin-dependent protein kinase II and nestin. As neither of these neuronal deletions of Sirt1 had impaired FAA, we then tested 1) a broad postnatal tamoxifen-inducible deletion, 2) a complete, developmental knockout of Sirt1, and 3) a gene replacement, catalytically inactive, form of Sirt1; but all of these mice had FAA similar to controls. Therefore, our findings suggest that FAA is completely independent of Sirt1.

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Additional Information:© 2018 Assali et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Received: November 19, 2017; Accepted: June 11, 2018; Published: June 25, 2018. Data Availability Statement: Data from this study are provided as a supplement. ADS received salary support from from the Ellison Medical Foundation and the Caltech Board Fellows in Brain Circuitry Program. This work was also supported by the Klarman Family Foundation and the Eli and Edythe Broad Foundation to ADS. Research reported in this publication was supported by the National Institute of General Medical Sciences of the National Institutes of Health under Award Number SC3GM125570. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. We thank Alex Paul, Daniel Chang, Vinita Khilnani, and Xinlin Yu (Caltech) for assistance with experiments; Dena Cohen and Lenny Guarente (MIT) for providing us with the floxed Sirt1 mice courtesy of Fred Alt (Harvard Medical School); Danica Chen (Univ. of California, Berkeley) for providing Sirt1 global knockout mouse brain tissue. Author Contributions: Conceptualization: Michael McBurney, Andrew D. Steele. Data curation: Cynthia T. Hsu, Keith M. Gunapala, Andrew D. Steele. Formal analysis: Dina R. Assali, Cynthia T. Hsu, Andrew D. Steele. Funding acquisition: Andrew D. Steele. Investigation: Dina R. Assali, Cynthia T. Hsu, Keith M. Gunapala, Antonio Aguayo, Andrew D. Steele. Methodology: Andrew D. Steele. Project administration: Dina R. Assali, Cynthia T. Hsu, Keith M. Gunapala, Andrew D. Steele. Resources: Antonio Aguayo, Michael McBurney. Software: Cynthia T. Hsu. Writing ± original draft: Andrew D. Steele. Writing ± review & editing: Dina R. Assali, Cynthia T. Hsu, Michael McBurney. The authors have declared that no competing interests exist.
Funding AgencyGrant Number
Ellison Medical FoundationUNSPECIFIED
Klarman Family FoundationUNSPECIFIED
Eli and Edythe Broad FoundationUNSPECIFIED
Issue or Number:6
PubMed Central ID:PMC6016907
Record Number:CaltechAUTHORS:20180702-090755831
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Official Citation:Assali DR, Hsu CT, Gunapala KM, Aguayo A, McBurney M, Steele AD (2018) Food anticipatory activity on a calorie-restricted diet is independent of Sirt1. PLoS ONE 13(6): e0199586.
Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:87508
Deposited By: Tony Diaz
Deposited On:03 Jul 2018 18:17
Last Modified:10 Feb 2020 21:56

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