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Start Over Author "Puigserver, Pere" Journal cell metabolism
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8. Adipose Tissue CLK2 Promotes Energy Expenditure during High-Fat Diet Intermittent Fasting

Author

Francisco Verdeguer, Mitsuhisa Tabata, Kfir Sharabi, Amy K. Rines, Pere Puigserver, Christian Trautwein, Chi Luo, Maximilian Hatting, Jessica A. Hall, University of Zurich, and Puigserver, Pere

Subjects
0301 basic medicine, Physiology, Adipose tissue, Diet induced thermogenesis, 1307 Cell Biology, 0302 clinical medicine, Adipose Tissue, Brown, Brown adipose tissue, Intermittent fasting, Protein Phosphatase 2, Phosphorylation, Cyclic AMP Response Element-Binding Protein, Uncoupling Protein 1, Mice, Knockout, biology, CREB, Kinase, brown fat, high, Fasting, Protein-Tyrosine Kinases, 10226 Department of Molecular Mechanisms of Disease, fat diet, PP2A, Up-Regulation, medicine.anatomical_structure, Adipocytes, Brown, Adipose Tissue, Organ Specificity, Disease Progression, UCP1, medicine.medical_specialty, induced thermogenesis, CLK2, Protein Serine-Threonine Kinases, Diet, High-Fat, Article, Dephosphorylation, 03 medical and health sciences, Oxygen Consumption, Internal medicine, 1312 Molecular Biology, medicine, Animals, Obesity, Molecular Biology, refeeding, intermittent fasting, 1314 Physiology, Cell Biology, Feeding Behavior, 030104 developmental biology, Endocrinology, biology.protein, 570 Life sciences, diet, Energy Metabolism, Thermogenesis, 030217 neurology & neurosurgery
Abstract

A promising approach to treating obesity is to increase diet-induced thermogenesis in brown adipose tissue (BAT), but the regulation of this process remains unclear. Here we find that CDC-like kinase 2 (CLK2) is expressed in BAT and upregulated upon refeeding. Mice lacking CLK2 in adipose tissue exhibit exacerbated obesity and decreased energy expenditure during high-fat diet intermittent fasting. Additionally, tissue oxygen consumption and protein levels of UCP1 are reduced in CLK2-deficient BAT. Phosphorylation of CREB, a transcriptional activator of UCP1, is markedly decreased in BAT cells lacking CLK2 due to enhanced CREB dephosphorylation. Mechanistically, CREB dephosphorylation is rescued by the inhibition of PP2A, a phosphatase that targets CREB. Our results suggest that CLK2 is a regulatory component of diet-induced thermogenesis in BAT through increased CREB-dependent expression of UCP1.

Published
2016

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