BROWSE

Related Researcher

Author's Photo

Suh, Pann-Ghill
BioSignal Network Lab (BSN)
Research Interests
  • Signal transduction, cancer, metabolism, phospholipase C

ITEM VIEW & DOWNLOAD

Obesity resistance and increased energy expenditure by white adipose tissue browning in Oga +/- mice.

DC Field Value Language
dc.contributor.author Yang, Yong Ryoul ko
dc.contributor.author Jang, Hyun-Jun ko
dc.contributor.author Choi, Sun-Sil ko
dc.contributor.author Lee, Yong Hwa ko
dc.contributor.author Lee, Gyun Hul ko
dc.contributor.author Seo, Young-Kyo ko
dc.contributor.author Choi, Jang Hyun ko
dc.contributor.author Park, Dohyun ko
dc.contributor.author Koh, Ara ko
dc.contributor.author Kim, Il Shin ko
dc.contributor.author Lee, Ho ko
dc.contributor.author Ryu, Sung Ho ko
dc.contributor.author Suh, Pann-Ghill ko
dc.date.available 2015-11-05T07:22:37Z -
dc.date.created 2015-11-02 ko
dc.date.issued 2015-12 ko
dc.identifier.citation DIABETOLOGIA, v.58, no.12, pp.2867 - 2876 ko
dc.identifier.issn 0012-186X ko
dc.identifier.uri https://scholarworks.unist.ac.kr/handle/201301/17698 -
dc.description.abstract Aims/hypothesis O-GlcNAcylation plays a role as a metabolic sensor regulating cellular signalling, transcription and metabolism. Transcription factors and signalling pathways related to metabolism are modulated by N-acetyl-glucosamine (O-GlcNAc) modification. Aberrant regulation of O-GlcNAcylation is closely linked to insulin resistance, type 2 diabetes and obesity. Current evidence shows that increased O-GlcNAcylation negatively regulates insulin signalling, which is associated with insulin resistance and type 2 diabetes. Here, we aimed to evaluate the effects of Oga (also known as Mgea5) haploinsufficiency, which causes hyper-O-GlcNAcylation, on metabolism. Methods We examined whether Oga +/- mice developed insulin resistance. Metabolic variables were determined including body weight, glucose and insulin tolerance, metabolic rate and thermogenesis. Results Oga deficiency does not affect insulin signalling even at hyper-O-GlcNAc levels. Oga +/- mice are lean with reduced fat mass and improved glucose tolerance. Furthermore, Oga +/- mice resist high-fat diet-induced obesity with ameliorated hepatic steatosis and improved glucose metabolism. Oga haploinsufficiency potentiates energy expenditure through the enhancement of brown adipocyte differentiation from the stromal vascular fraction of subcutaneous white adipose tissue (WAT). Conclusions/interpretation Our observations suggest that O-GlcNAcase (OGA) is essential for energy metabolism via regulation of the thermogenic WAT program. ko
dc.description.statementofresponsibility close -
dc.language 영어 ko
dc.publisher SPRINGER ko
dc.title Obesity resistance and increased energy expenditure by white adipose tissue browning in Oga +/- mice. ko
dc.type ARTICLE ko
dc.identifier.scopusid 2-s2.0-84946500719 ko
dc.identifier.wosid 000364221200021 ko
dc.type.rims ART ko
dc.description.wostc 0 *
dc.description.scopustc 0 *
dc.date.tcdate 2015-12-28 *
dc.identifier.doi 10.1007/s00125-015-3736-z ko
dc.identifier.url http://link.springer.com/article/10.1007%2Fs00125-015-3736-z ko
Appears in Collections:
BIO_Journal Papers
Files in This Item:
There are no files associated with this item.

find_unist can give you direct access to the published full text of this article. (UNISTARs only)

Show simple item record

qrcode

  • mendeley

    citeulike

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

MENU