DNA Methylation Suppresses Leptin Gene in 3T3-L1 Adipocytes 11 8

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DNA Methylation Suppresses Leptin Gene in 3T3-L1 Adipocytes 8

Persistent ID (NDL): info:ndljp/pid/10993566

Material type: 博士論文

Author: Kuroda, Masashiほか

Publisher: PLOS

Publication date: 2016-08-05

Material Format: Digital

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Name of awarding university/degree: 徳島大学,博士（栄養学）

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Note (General)：: Leptin is a key regulator of energy intake and expenditure. This peptide hormone is expressed in mouse white adipose tissue, but hardly expressed in 3...

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Material Type: 博士論文
ISSN: 1932-6203
Title: DNA Methylation Suppresses Leptin Gene in 3T3-L1 Adipocytes
Volume: 11 8
Author/Editor: Kuroda, Masashi
Tominaga, Ayako
Nakagawa, Kasumi
Nishiguchi, Misa
Sebe, Mayu
Miyatake, Yumiko
Kitamura, Tadahiro
Tsutsumi, Rie
Harada, Nagakatsu
Nakaya, Yutaka
Sakaue, Hiroshi
Author Heading: Kuroda, Masashi
Tominaga, Ayako
Nakagawa, Kasumi
Nishiguchi, Misa
Sebe, Mayu
Miyatake, Yumiko
Kitamura, Tadahiro
Tsutsumi, Rie
Harada, Nagakatsu
Nakaya, Yutaka
Sakaue, Hiroshi
Publication, Distribution, etc.: PLOS
Publication Date: 2016-08-05
Publication Date (W3CDTF): 2016-08-05
Alternative Title: DNAメチル化は3T3-L1脂肪細胞におけるレプチン発現を抑制する
DNA Methylation Suppresses Leptin Expression in Adipocytes
Periodical title: PLOS ONE
Degree grantor/type: 徳島大学
Date Granted: 2017-03-23
Date Granted (W3CDTF): 2017-03-23
Dissertation Number: 甲第3087号
Degree Type: 博士（栄養学）
Conferring No. (Dissertation): 甲第3087号
Text Language Code: eng
Subject Heading: Adipocyte
Leptin
DNA methylation
3T3-L1
obesity
Target Audience: 一般
Note (General): Leptin is a key regulator of energy intake and expenditure. This peptide hormone is expressed in mouse white adipose tissue, but hardly expressed in 3T3-L1 adipocytes. Using bisulfite sequencing, we found that CpG islands in the leptin promoter are highly methylated in 3T3-L1cells. 5-azacytidine, an inhibitor of DNA methyltransferase, markedly increased leptin expression as pre-adipocytes matured into adipocytes. Remarkably, leptin expression was stimulated by insulin in adipocytes derived from precursor cells exposed to 5-azacytidine, but suppressed by thiazolidinedione and dexamethasone. In contrast, adipocytes derived from untreated precursor cells were unresponsive to both 5-azacytidine and hormonal stimuli, although lipid accumulation was sufficient to boost leptin expression in the absence of demethylation. Taken together, the results suggest that leptin expression in 3T3-L1 cells requires DNA demethylation prior to adipogenesis, transcriptional activation during adipogenesis, and lipid accumulation after adipogenesis.
DOI: info:doi/10.1371/journal.pone.0160532
https://doi.org/info:doi/10.1371/journal.pone.0160532
Persistent ID (NDL): info:ndljp/pid/10993566
https://dl.ndl.go.jp/pid/10993566
Collection: 障害者向け資料
Collection (Materials For Handicapped People:1): テキストデータ
Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文
https://dl.ndl.go.jp/collections/A00014
Acquisition Basis: 博士論文（自動収集）
Date Accepted (W3CDTF): 2017-12-04T02:02:48+09:00
Format (IMT): application/pdf
Access Restrictions: 国立国会図書館内限定公開
Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
Availability of remote photoduplication service: 可
Periodical Title (URI): http://repo.lib.tokushima-u.ac.jp/110107
Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション
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