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Specific SIRT1 Activation Mimics Low Energy Levels and Protects against Diet-Induced Metabolic Disorders by Enhancing Fat Oxidation

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TLDR
The metabolic phenotype of mice treated with SRT1720, a specific and potent synthetic activator of SIRT1 that is devoid of direct action on AMPK that robustly enhances endurance running performance and strongly protects from diet-induced obesity and insulin resistance by enhancing oxidative metabolism in skeletal muscle, liver, and brown adipose tissue is reported.
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This article is published in Cell Metabolism.The article was published on 2008-11-05 and is currently open access. It has received 702 citations till now. The article focuses on the topics: AMPK & SRT1720.

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The Hallmarks of Aging

TL;DR: Nine tentative hallmarks that represent common denominators of aging in different organisms are enumerated, with special emphasis on mammalian aging, to identify pharmaceutical targets to improve human health during aging, with minimal side effects.
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AMPK regulates energy expenditure by modulating NAD + metabolism and SIRT1 activity

TL;DR: It is demonstrated that AMPK controls the expression of genes involved in energy metabolism in mouse skeletal muscle by acting in coordination with another metabolic sensor, the NAD+-dependent type III deacetylase SIRT1.
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Mammalian sirtuins: biological insights and disease relevance.

TL;DR: There have been major advances in the understanding of the enzymology of sirtuins, their regulation, and their ability to broadly improve mammalian physiology and health span, and the challenges that will confront the field in the coming years are discussed.
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Sirtuins as regulators of metabolism and healthspan

TL;DR: The mammalian sirtuin protein family (comprising SIRT1–SIRT7) has received much attention for its regulatory role, mainly in metabolism and ageing, thereby acting as crucial regulators of the network that controls energy homeostasis and as such determines healthspan.
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TGR5-Mediated Bile Acid Sensing Controls Glucose Homeostasis

TL;DR: It is shown here that TGR5 signaling induces intestinal glucagon-like peptide-1 (GLP-1) release, leading to improved liver and pancreatic function and enhanced glucose tolerance in obese mice, and suggested that pharmacological targeting of T GR5 may constitute a promising incretin-based strategy for the treatment of diabesity and associated metabolic disorders.
References
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Resveratrol improves mitochondrial function and protects against metabolic disease by activating SIRT1 and PGC-1alpha.

TL;DR: RSV's effects were associated with an induction of genes for oxidative phosphorylation and mitochondrial biogenesis and were largely explained by an RSV-mediated decrease in P GC-1alpha acetylation and an increase in PGC-1 alpha activity.
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Nutrient control of glucose homeostasis through a complex of PGC-1alpha and SIRT1.

TL;DR: It is shown that the Sir2 homologue, SIRT1 controls the gluconeogenic/glycolytic pathways in liver in response to fasting signals through the transcriptional coactivator PGC-1α, and this findings have strong implications for the basic pathways of energy homeostasis, diabetes and lifespan.
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hSIR2SIRT1 Functions as an NAD-Dependent p53 Deacetylase

TL;DR: It is proposed that hSir2, the human homolog of the S. cerevisiae Sir2 protein known to be involved in cell aging and in the response to DNA damage, binds and deacetylates the p53 protein with a specificity for its C-terminal Lys382 residue.
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Transcriptional co-activator PGC-1α drives the formation of slow-twitch muscle fibres

TL;DR: Using fibre-type-specific promoters, it is shown in cultured muscle cells that PGC-1α activates transcription in cooperation with Mef2 proteins and serves as a target for calcineurin signalling, which has been implicated in slow fibre gene expression.
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