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

Collection with item attached
2017
Item details URL
http://open-repository.kisti.re.kr/cube/handle/open_repository/487007.do
DOI
10.1038/srep40445
Title
White to beige conversion in PDE3B KO adipose tissue through activationof AMPK signaling and mitochondrial function
Description
We thank Dr. Bruce M. Spiegelman for providing PGC-1 alpha adenovirus,which was used to infect H4IIE hepatoma cells to produce PGC-1 alphaprotein. We also acknowledge the NIDDK Mouse Metabolism Core forindirect calorimetry data. This work was supported in part by theIntramural Research Programs (NIH/NHLBI and NIDDK). Y.W.C. was supportedby the Basic Science Research Program through the National ResearchFoundation of Korea (NRF), funded by the Ministry of Education(NRF-2015R1D1A1A01057981). K.B. and E.D. were supported by the SwedishDiabetes Society and the Albert Pahlsson Foundation, DIA 2014-031 andDIA 2014-2832, respectively. Dr. Manganiello died prior to completion ofthe manuscript. Joel Moss, a long-time colleague, assisted with reviewof the data and completion of the manuscript.
abstract
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 beta-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.
provenance
Made available in Cube on 2018-09-28T16:22:46Z (GMT). No. of bitstreams: 0
language
English
author
Chung, Youn Wook
Ahmad, Faiyaz
Tang, Yan
Hockman, Steven C.
Kee, Hyun Jung
Berger, Karin
Guirguis, Emilia
Choi, Young Hun
Schimel, Dan M.
Aponte, Angel M.
Park, Sunhee
Degerman, Eva
Manganiello, Vincent C.
accessioned
2018-09-28T16:22:46Z
available
2018-09-28T16:22:46Z
issued
2017
citation
SCIENTIFIC REPORTS(7)
issn
2045-2322
uri
http://open-repository.kisti.re.kr/cube/handle/open_repository/487007.do
Funder
교육부
Funding Program
개인기초연구(교육부)
Project ID
1345270918
Jurisdiction
Rep.of Korea
Project Name
Functional Study of Mitochondria and Its Regulatory Mechanism in Beige Fat Activation Using PDE3B KO Mouse Model
rights
openAccess
type
article


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