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Zachary Gerhart-Hines

Researcher at University of Copenhagen

Publications -  53
Citations -  7910

Zachary Gerhart-Hines is an academic researcher from University of Copenhagen. The author has contributed to research in topics: Thermogenesis & Adipose tissue. The author has an hindex of 21, co-authored 35 publications receiving 6640 citations. Previous affiliations of Zachary Gerhart-Hines include University of Pennsylvania & Johns Hopkins University School of Medicine.

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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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Metabolic control of muscle mitochondrial function and fatty acid oxidation through SIRT1/PGC‐1α

TL;DR: SIRT1 is identified as a functional regulator of PGC‐1α that induces a metabolic gene transcription program of mitochondrial fatty acid oxidation in response to low glucose concentrations and has implications for understanding selective nutrient adaptation and how it might impact lifespan or metabolic diseases such as obesity and diabetes.
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Antioxidant and Oncogene Rescue of Metabolic Defects Caused by Loss of Matrix Attachment

TL;DR: The results show both the importance of matrix attachment in regulating metabolic activity and an unanticipated mechanism for cell survival in altered matrix environments by antioxidant restoration of ATP generation by antioxidant treatment.
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Metabolic adaptations through the PGC-1α and SIRT1 pathways

TL;DR: Understanding the PGC‐1α and SIRT1 pathways might have important implications for comprehending metabolic and age‐associated diseases.
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The cAMP/PKA Pathway Rapidly Activates SIRT1 to Promote Fatty Acid Oxidation Independently of Changes in NAD +

TL;DR: A cAMP-induced phosphorylation of a highly conserved serine (S434) located in the SIRT1 catalytic domain that rapidly enhanced intrinsic deacetylase activity independently of changes in NAD(+) levels is identified.