Document Detail


Increased mitochondrial activity in BMP7-treated brown adipocytes, due to increased CPT1- and CD36-mediated fatty acid uptake.
MedLine Citation:
PMID:  22938691     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
AIMS: Brown adipose tissue dissipates chemical energy in the form of heat and regulates triglyceride and glucose metabolism in the body. Factors that regulate fatty acid uptake and oxidation in brown adipocytes have not yet been fully elucidated. Bone morphogenetic protein 7 (BMP7) is a growth factor capable of inducing brown fat mitochondrial biogenesis during differentiation from adipocyte progenitors. Administration of BMP7 to mice also results in increased energy expenditure. To determine if BMP7 is able to affect the mitochondrial activity of mature brown adipocytes, independent of the differentiation process, we delivered BMP7 to mature brown adipocytes and measured mitochondrial activity.
RESULTS: We found that BMP7 increased mitochondrial activity, including fatty acid oxidation and citrate synthase activity, without increasing the mitochondrial number. This was accompanied by an increase in fatty acid uptake and increased protein expression of CPT1 and CD36, which import fatty acids into the mitochondria and the cell, respectively. Importantly, inhibition of either CPT1 or CD36 resulted in a blunting of the mitochondrial activity of BMP7-treated cells.
INNOVATION: These findings uncover a novel pathway regulating mitochondrial activities in mature brown adipocytes by BMP7-mediated fatty acid uptake and oxidation.
CONCLUSION: In conclusion, BMP7 increases mitochondrial activity in mature brown adipocytes via increased fatty acid uptake and oxidation, a process that requires the fatty acid transporters CPT1 and CD36.
Authors:
Kristy L Townsend; Ding An; Matthew D Lynes; Tian Lian Huang; Hongbin Zhang; Laurie J Goodyear; Yu-Hua Tseng
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-10-09
Journal Detail:
Title:  Antioxidants & redox signaling     Volume:  19     ISSN:  1557-7716     ISO Abbreviation:  Antioxid. Redox Signal.     Publication Date:  2013 Jul 
Date Detail:
Created Date:  2013-06-26     Completed Date:  2014-01-24     Revised Date:  2014-07-21    
Medline Journal Info:
Nlm Unique ID:  100888899     Medline TA:  Antioxid Redox Signal     Country:  United States    
Other Details:
Languages:  eng     Pagination:  243-57     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Activating Transcription Factor 2 / metabolism
Adenosine Triphosphate / metabolism
Adipocytes, Brown / metabolism*
Adipose Tissue, Brown / metabolism
Animals
Antigens, CD36 / metabolism*
Biological Transport
Body Temperature
Bone Morphogenetic Protein 7 / genetics,  metabolism*
Carnitine O-Palmitoyltransferase / metabolism*
Catalysis
Cell Respiration
Energy Metabolism
Fatty Acids / metabolism*
Gene Expression
Mice
Mitochondria / metabolism*
Models, Biological
Oxidation-Reduction
Pyruvic Acid / metabolism
Smad Proteins, Receptor-Regulated / metabolism
Transfection
p38 Mitogen-Activated Protein Kinases / metabolism
Grant Support
ID/Acronym/Agency:
F32 DK091996/DK/NIDDK NIH HHS; P30 DK036836/DK/NIDDK NIH HHS; R01 DK077097/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Activating Transcription Factor 2; 0/Antigens, CD36; 0/Bone Morphogenetic Protein 7; 0/Fatty Acids; 0/Smad Proteins, Receptor-Regulated; 8558G7RUTR/Pyruvic Acid; 8L70Q75FXE/Adenosine Triphosphate; EC 2.3.1.21/Carnitine O-Palmitoyltransferase; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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