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White to beige conversion in PDE3B KO adipose tissue through activation of AMPK signaling and mitochondrial function

Author:
  • Youn Wook Chung
  • Faiyaz Ahmad
  • Yan Tang
  • Steven C. Hockman
  • Hyun Jung Kee
  • Karin Berger
  • Emilia Guirguis
  • Young Hun Choi
  • Dan M. Schimel
  • Angel M. Aponte
  • Sunhee Park
  • Eva Degerman
  • Vincent C Manganiello
Publishing year: 2017-01-13
Language: English
Publication/Series: Scientific Reports
Volume: 7
Document type: Journal article
Publisher: Nature Publishing Group

Abstract english

Understanding mechanisms by which a population of beige adipocytes is increased in white adipose tissue (WAT) reflects a potential strategy in the fight against obesity and diabetes. Cyclic adenosine monophosphate (cAMP) is very important in the development of the beige phenotype and activation of its thermogenic program. To study effects of cyclic nucleotides on energy homeostatic mechanisms, mice were generated by targeted inactivation of cyclic nucleotide phosphodiesterase 3b (Pde3b) gene, which encodes PDE3B, an enzyme that catalyzes hydrolysis of cAMP and cGMP and is highly expressed in tissues that regulate energy homeostasis, including adipose tissue, liver, and pancreas. In epididymal white adipose tissue (eWAT) of PDE3B KO mice on a SvJ129 background, cAMP/protein kinase A (PKA) and AMP-activated protein kinase (AMPK) signaling pathways are activated, resulting in "browning" phenotype, with a smaller increases in body weight under high-fat diet, smaller fat deposits, increased β-oxidation of fatty acids (FAO) and oxygen consumption. Results reported here suggest that PDE3B and/or its downstream signaling partners might be important regulators of energy metabolism in adipose tissue, and potential therapeutic targets for treating obesity, diabetes and their associated metabolic disorders.

Keywords

  • Endocrinology and Diabetes

Other

Published
  • Molecular Nutrition
  • Insulin Signal Transduction
  • ISSN: 2045-2322
Eva Degerman
E-mail: eva [dot] degerman [at] med [dot] lu [dot] se

Professor

Insulin Signal Transduction

+46 46 222 85 83

+46 70 885 83 62

BMC C1121b

66

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