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Zinc transporter ZIP13 suppresses beige adipocyte biogenesis and energy expenditure by regulating C/EBP-β expression.

Abstract Given the relevance of beige adipocytes in adult humans, a better understanding of the molecular circuits involved in beige adipocyte biogenesis has provided new insight into human brown adipocyte biology. Genetic mutations in SLC39A13/ZIP13, a member of zinc transporter family, are known to reduce adipose tissue mass in humans; however, the underlying mechanisms remains unknown. Here, we demonstrate that the Zip13-deficient mouse shows enhanced beige adipocyte biogenesis and energy expenditure, and shows ameliorated diet-induced obesity and insulin resistance. Both gain- and loss-of-function studies showed that an accumulation of the CCAAT/enhancer binding protein-β (C/EBP-β) protein, which cooperates with dominant transcriptional co-regulator PR domain containing 16 (PRDM16) to determine brown/beige adipocyte lineage, is essential for the enhanced adipocyte browning caused by the loss of ZIP13. Furthermore, ZIP13-mediated zinc transport is a prerequisite for degrading the C/EBP-β protein to inhibit adipocyte browning. Thus, our data reveal an unexpected association between zinc homeostasis and beige adipocyte biogenesis, which may contribute significantly to the development of new therapies for obesity and metabolic syndrome.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title plos genetics
Publication Year Start




PMID- 28854265
OWN - NLM
STAT- MEDLINE
DA  - 20170830
DCOM- 20170912
LR  - 20170917
IS  - 1553-7404 (Electronic)
IS  - 1553-7390 (Linking)
VI  - 13
IP  - 8
DP  - 2017 Aug
TI  - Zinc transporter ZIP13 suppresses beige adipocyte biogenesis and energy
      expenditure by regulating C/EBP-beta expression.
PG  - e1006950
LID - 10.1371/journal.pgen.1006950 [doi]
AB  - Given the relevance of beige adipocytes in adult humans, a better understanding
      of the molecular circuits involved in beige adipocyte biogenesis has provided new
      insight into human brown adipocyte biology. Genetic mutations in SLC39A13/ZIP13, 
      a member of zinc transporter family, are known to reduce adipose tissue mass in
      humans; however, the underlying mechanisms remains unknown. Here, we demonstrate 
      that the Zip13-deficient mouse shows enhanced beige adipocyte biogenesis and
      energy expenditure, and shows ameliorated diet-induced obesity and insulin
      resistance. Both gain- and loss-of-function studies showed that an accumulation
      of the CCAAT/enhancer binding protein-beta (C/EBP-beta) protein, which cooperates
      with dominant transcriptional co-regulator PR domain containing 16 (PRDM16) to
      determine brown/beige adipocyte lineage, is essential for the enhanced adipocyte 
      browning caused by the loss of ZIP13. Furthermore, ZIP13-mediated zinc transport 
      is a prerequisite for degrading the C/EBP-beta protein to inhibit adipocyte
      browning. Thus, our data reveal an unexpected association between zinc
      homeostasis and beige adipocyte biogenesis, which may contribute significantly to
      the development of new therapies for obesity and metabolic syndrome.
FAU - Fukunaka, Ayako
AU  - Fukunaka A
AD  - Department of Metabolism & Endocrinology, Juntendo University Graduate School of 
      Medicine, Tokyo, Japan.
AD  - Laboratory of Developmental Biology & Metabolism, Institute for Molecular &
      Cellular Regulation, Gunma University, Maebashi, Gunma, Japan.
AD  - AMED-JST-CREST Program, Tokyo, Japan.
FAU - Fukada, Toshiyuki
AU  - Fukada T
AD  - Faculty of Pharmaceutical Sciences, Tokushima Bunri University, Tokushima, Japan.
AD  - Division of Pathology, Department of Oral Diagnostic Sciences, School of
      Dentistry, Showa University, Tokyo, Japan.
AD  - RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
FAU - Bhin, Jinhyuk
AU  - Bhin J
AD  - Department of Molecular Carcinogenesis, The Netherlands Cancer Institute,
      Amsterdam, The Netherlands.
FAU - Suzuki, Luka
AU  - Suzuki L
AD  - Department of Metabolism & Endocrinology, Juntendo University Graduate School of 
      Medicine, Tokyo, Japan.
FAU - Tsuzuki, Takamasa
AU  - Tsuzuki T
AD  - Graduate School of Health and Sports Science, Juntendo University, Inzai, Chiba, 
      Japan.
FAU - Takamine, Yuri
AU  - Takamine Y
AD  - Graduate School of Health and Sports Science, Juntendo University, Inzai, Chiba, 
      Japan.
FAU - Bin, Bum-Ho
AU  - Bin BH
AD  - Division of Pathology, Department of Oral Diagnostic Sciences, School of
      Dentistry, Showa University, Tokyo, Japan.
FAU - Yoshihara, Toshinori
AU  - Yoshihara T
AUID- ORCID: http://orcid.org/0000-0002-8465-5439
AD  - Graduate School of Health and Sports Science, Juntendo University, Inzai, Chiba, 
      Japan.
FAU - Ichinoseki-Sekine, Noriko
AU  - Ichinoseki-Sekine N
AUID- ORCID: http://orcid.org/0000-0002-0467-3312
AD  - Graduate School of Health and Sports Science, Juntendo University, Inzai, Chiba, 
      Japan.
FAU - Naito, Hisashi
AU  - Naito H
AD  - Graduate School of Health and Sports Science, Juntendo University, Inzai, Chiba, 
      Japan.
FAU - Miyatsuka, Takeshi
AU  - Miyatsuka T
AD  - Department of Metabolism & Endocrinology, Juntendo University Graduate School of 
      Medicine, Tokyo, Japan.
FAU - Takamiya, Shinzaburo
AU  - Takamiya S
AD  - Department of Tropical Medicine and Parasitology, Graduate School of Medicine,
      Juntendo University, Tokyo, Japan.
FAU - Sasaki, Tsutomu
AU  - Sasaki T
AD  - Laboratory of Metabolic Signaling, Institute for Molecular & Cellular Regulation,
      Gunma University, Maebashi, Gunma, Japan.
FAU - Inagaki, Takeshi
AU  - Inagaki T
AD  - Laboratory of Epigenetics and Metabolism, Institute for Molecular & Cellular
      Regulation, Gunma University, Maebashi, Gunma, Japan.
FAU - Kitamura, Tadahiro
AU  - Kitamura T
AD  - Laboratory of Metabolic Signaling, Institute for Molecular & Cellular Regulation,
      Gunma University, Maebashi, Gunma, Japan.
FAU - Kajimura, Shingo
AU  - Kajimura S
AD  - UCSF Diabetes Center and Department of Cell and Tissue Biology, University of
      California-San Francisco, San Francisco, United States of America.
AD  - PRESTO-JST, Tokyo, Japan.
FAU - Watada, Hirotaka
AU  - Watada H
AD  - Department of Metabolism & Endocrinology, Juntendo University Graduate School of 
      Medicine, Tokyo, Japan.
AD  - Center for Identification of Diabetic Therapeutic Targets, Juntendo University
      Graduate School of Medicine, Tokyo, Japan.
AD  - Sportology Center, Juntendo University Graduate School of Medicine, Tokyo, Japan.
AD  - Center for Therapeutic Innovations in Diabetes, Juntendo University Graduate
      School of Medicine, Tokyo, Japan.
FAU - Fujitani, Yoshio
AU  - Fujitani Y
AUID- ORCID: http://orcid.org/0000-0003-0196-4736
AD  - Department of Metabolism & Endocrinology, Juntendo University Graduate School of 
      Medicine, Tokyo, Japan.
AD  - Laboratory of Developmental Biology & Metabolism, Institute for Molecular &
      Cellular Regulation, Gunma University, Maebashi, Gunma, Japan.
AD  - AMED-JST-CREST Program, Tokyo, Japan.
AD  - Center for Therapeutic Innovations in Diabetes, Juntendo University Graduate
      School of Medicine, Tokyo, Japan.
LA  - eng
PT  - Journal Article
DEP - 20170830
PL  - United States
TA  - PLoS Genet
JT  - PLoS genetics
JID - 101239074
RN  - 0 (CCAAT-Enhancer-Binding Protein-beta)
RN  - 0 (Cation Transport Proteins)
RN  - 0 (Cebpb protein, mouse)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Prdm16 protein, mouse)
RN  - 0 (Slc39a13 protein, mouse)
RN  - 0 (Transcription Factors)
RN  - J41CSQ7QDS (Zinc)
SB  - IM
MH  - Adipocytes, Beige/metabolism
MH  - Adipogenesis/genetics
MH  - Animals
MH  - CCAAT-Enhancer-Binding Protein-beta/*genetics
MH  - Cation Transport Proteins/*genetics/metabolism
MH  - Cell Lineage
MH  - DNA-Binding Proteins/*genetics/metabolism
MH  - Diet, High-Fat
MH  - Energy Metabolism/genetics
MH  - Humans
MH  - Insulin Resistance/genetics
MH  - Mice
MH  - Mice, Knockout
MH  - Obesity/*genetics/metabolism/pathology
MH  - Transcription Factors/*genetics/metabolism
MH  - Zinc/metabolism
PMC - PMC5576661
EDAT- 2017/08/31 06:00
MHDA- 2017/09/13 06:00
CRDT- 2017/08/31 06:00
PHST- 2016/10/06 [received]
PHST- 2017/07/31 [accepted]
AID - 10.1371/journal.pgen.1006950 [doi]
AID - PGENETICS-D-16-02231 [pii]
PST - epublish
SO  - PLoS Genet. 2017 Aug 30;13(8):e1006950. doi: 10.1371/journal.pgen.1006950.
      eCollection 2017 Aug.