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BNIP3 is essential for mitochondrial bioenergetics during adipocyte remodelling in mice

Authors
 Jin Woo Choi  ;  Anna Jo  ;  Min Kim  ;  Ho Seon Park  ;  Sung Soo Chung  ;  Shinae Kang  ;  Kyong Soo Park 
Citation
 DIABETOLOGIA, Vol.59(3) : 571-581, 2016 
Journal Title
 DIABETOLOGIA 
ISSN
 0012-186X 
Issue Date
2016
MeSH
3T3-L1 Cells ; Adipocytes/drug effects ; Adipocytes/metabolism* ; Animals ; Blotting, Western ; Electrophoretic Mobility Shift Assay ; Energy Metabolism/drug effects ; Membrane Proteins/metabolism* ; Mice ; Mice, Inbred C57BL ; Mitochondria/drug effects ; Mitochondria/metabolism* ; Mitochondrial Proteins/metabolism* ; PPAR gamma/pharmacology ; Polymerase Chain Reaction
Keywords
Adipocytes ; BNIP3 ; Bioenergetics ; Insulin resistance ; Mitochondria ; PPRE ; Rosiglitazone
Abstract
AIMS/HYPOTHESIS: Adipose tissue is a highly versatile system in which mitochondria in adipocytes undergo significant changes during active tissue remodelling. BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3) is a mitochondrial protein and a known mitochondrial quality regulator. In this study, we investigated the role of BNIP3 in adipocytes, specifically under conditions of peroxisome proliferator-activated receptor-γ (PPARγ)-induced adipose tissue remodelling. METHODS: The expression of BNIP3 was evaluated in 3T3-L1 adipocytes in vitro, C57BL/6 mice fed a high-fat diet and db/db mice in vivo. Mitochondrial bioenergetics was investigated in BNIP3-knockdown adipocytes after rosiglitazone treatment. A putative peroxisome proliferator hormone responsive element (PPRE) was characterised by promoter assay and electrophoretic mobility shift assay (EMSA). RESULTS: The protein BNIP3 was more abundant in brown adipose tissue than white adipose tissue. Furthermore, BNIP3 expression was upregulated by 3T3-L1 pre-adipocyte differentiation, starvation and rosiglitazone treatment. Conversely, BNIP3 expression in adipocytes decreased under various conditions associated with insulin resistance. This downregulation of BNIP3 was restored by rosiglitazone treatment. Knockdown of BNIP3 in adipocytes inhibited rosiglitazone-induced mitochondrial biogenesis and function, partially mediated by the 5' AMP-activated protein kinase (AMPK)-peroxisome proliferator-activated receptor γ, co-activator 1 α (PGC1α) signalling pathway. Rosiglitazone treatment increased the transcription level of Bnip3 in the reporter assay and the presence of the PPRE site in the Bnip3 promoter was demonstrated by EMSA. CONCLUSIONS/INTERPRETATION: The protein BNIP3 contributes to the improvement of mitochondrial bioenergetics that occurs on exposure to rosiglitazone. It may be a novel therapeutic target for restoring mitochondrial dysfunction under insulin-resistant conditions.
Full Text
http://link.springer.com/article/10.1007/s00125-015-3836-9
DOI
10.1007/s00125-015-3836-9
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Kang, Shin Ae(강신애) ORCID logo https://orcid.org/0000-0002-9719-4774
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/146343
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