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Dina Laznik-Bogoslavski

Researcher at Harvard University

Publications -  13
Citations -  2513

Dina Laznik-Bogoslavski is an academic researcher from Harvard University. The author has contributed to research in topics: Thermogenesis & Adipose tissue. The author has an hindex of 9, co-authored 12 publications receiving 1847 citations.

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Exercise induces hippocampal BDNF through a PGC-1α/FNDC5 pathway

TL;DR: It is shown that FNDC5, a previously identified muscle protein that is induced in exercise and is cleaved and secreted as irisin, is also elevated by endurance exercise in the hippocampus of mice.
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A Creatine-Driven Substrate Cycle Enhances Energy Expenditure and Thermogenesis in Beige Fat

TL;DR: It is demonstrated that creatine enhances respiration in beige-fat mitochondria when ADP is limiting and decreases whole-body energy expenditure after administration of a β3-agonist and reduces beige and brown adipose metabolic rate.
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Mitochondrial ROS regulate thermogenic energy expenditure and sulfenylation of UCP1

TL;DR: Mitochondrial ROS induction in brown adipose tissue is identified as a mechanism that supports UCP1-dependent thermogenesis and whole-body energy expenditure, which opens the way to improved therapeutic strategies for combating metabolic disorders.
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An ERK/Cdk5 axis controls the diabetogenic actions of PPARγ

TL;DR: Pharmacological inhibition of MEK and ERK markedly improves insulin resistance in both obese wild-type and ob/ob mice, and also completely reverses the deleterious effects of the Cdk5 ablation, suggesting that MEK/ERK inhibitors may hold promise for the treatment of type 2 diabetes.
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Genetic Depletion of Adipocyte Creatine Metabolism Inhibits Diet-Induced Thermogenesis and Drives Obesity

TL;DR: Inactivated the first and rate-limiting enzyme of creatine biosynthesis, glycine amidinotransferase (GATM), selectively in fat of Adipo-Gatm KO mice, providing strong in vivo genetic support for a role of GATM and creatine metabolism in energy expenditure, diet-induced thermogenesis, and defense against diet- induced obesity.