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Identification of KMU-3, a novel derivative of gallic acid, as an inhibitor of adipogenesis.

Differentiation of preadipocyte, also called adipogenesis, leads to the phenotype of mature adipocyte. Excessive adipogenesis, however, is largely linked to the development of obesity. Herein we investigated a library of 53 novel chemicals, generated from a number of polyphenolic natural compounds,... Full description

Journal Title: PloS one 2014, Vol.9(10), p.e109344
Main Author: Park, Yu-Kyoung
Other Authors: Lee, Jinho , Hong, Victor Sukbong , Choi, Jong-Soon , Lee, Tae-Yoon , Jang, Byeong-Churl
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0109344
Link: http://search.proquest.com/docview/1609306251/?pq-origsite=primo
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title: Identification of KMU-3, a novel derivative of gallic acid, as an inhibitor of adipogenesis.
format: Article
creator:
  • Park, Yu-Kyoung
  • Lee, Jinho
  • Hong, Victor Sukbong
  • Choi, Jong-Soon
  • Lee, Tae-Yoon
  • Jang, Byeong-Churl
subjects:
  • 3t3-L1 Cells–Cytology
  • Adipocytes–Drug Effects
  • Adipogenesis–Metabolism
  • Animals–Drug Effects
  • Benzamides–Chemical Synthesis
  • Ccaat-Enhancer-Binding Protein-Alpha–Pharmacology
  • Chemokine Ccl5–Genetics
  • Down-Regulation–Metabolism
  • Drug Evaluation, Preclinical–Genetics
  • Gallic Acid–Drug Effects
  • Leptin–Analogs & Derivatives
  • Mice–Chemical Synthesis
  • Ppar Gamma–Pharmacology
  • Phosphorylation–Genetics
  • RNA, Messenger–Genetics
  • Retinol-Binding Proteins, Plasma–Metabolism
  • Stat3 Transcription Factor–Drug Effects
  • Fas Receptor–Genetics
  • Fas Receptor
ispartof: PloS one, 2014, Vol.9(10), p.e109344
description: Differentiation of preadipocyte, also called adipogenesis, leads to the phenotype of mature adipocyte. Excessive adipogenesis, however, is largely linked to the development of obesity. Herein we investigated a library of 53 novel chemicals, generated from a number of polyphenolic natural compounds, on adipogenesis. Strikingly, among the chemicals tested, KMU-3, a derivative of gallic acid, strongly suppressed lipid accumulation during the differentiation of 3T3-L1 preadipocytes into adipocytes. On mechanistic levels, KMU-3 inhibited expressions of CCAAT/enhancer-binding protein-α (C/EBP-α), peroxisome proliferator-activated receptor-γ (PPAR-γ), and fatty acid synthase (FAS) during adipocyte differentiation. Moreover, KMU-3 reduced expressions of adipokines, including retinol binding protein-4 (RBP-4), leptin, and regulated on activation, normal T cell expressed and secreted (RANTES) during adipocyte differentiation. Of further note, KMU-3 rapidly blocked the phosphorylation of signal transducer and activator of transcription-3 (STAT-3) during the early stage of adipogenesis. Importantly, pharmacological inhibition studies revealed that AG490, a JAK-2/STAT-3 inhibitor suppressed adipogenesis and STAT-3 phosphorylation, implying that early blockage of STAT-3 activity is crucial for the KMU-3-mediated anti-adipogenesis. These findings demonstrate firstly that KMU-3 inhibits adipogenesis by down-regulating STAT-3, PPAR-γ, C/EBP-α, and FAS. This work shows that KMU-3 is an inhibitor of adipogenesis and thus may have therapeutic potential against obesity.
language: eng
source:
identifier: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0109344
fulltext: fulltext
issn:
  • 19326203
  • 1932-6203
url: Link


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titleIdentification of KMU-3, a novel derivative of gallic acid, as an inhibitor of adipogenesis.
creatorPark, Yu-Kyoung ; Lee, Jinho ; Hong, Victor Sukbong ; Choi, Jong-Soon ; Lee, Tae-Yoon ; Jang, Byeong-Churl
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identifierE-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0109344
subject3t3-L1 Cells–Cytology ; Adipocytes–Drug Effects ; Adipogenesis–Metabolism ; Animals–Drug Effects ; Benzamides–Chemical Synthesis ; Ccaat-Enhancer-Binding Protein-Alpha–Pharmacology ; Chemokine Ccl5–Genetics ; Down-Regulation–Metabolism ; Drug Evaluation, Preclinical–Genetics ; Gallic Acid–Drug Effects ; Leptin–Analogs & Derivatives ; Mice–Chemical Synthesis ; Ppar Gamma–Pharmacology ; Phosphorylation–Genetics ; RNA, Messenger–Genetics ; Retinol-Binding Proteins, Plasma–Metabolism ; Stat3 Transcription Factor–Drug Effects ; Fas Receptor–Genetics ; Fas Receptor
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descriptionDifferentiation of preadipocyte, also called adipogenesis, leads to the phenotype of mature adipocyte. Excessive adipogenesis, however, is largely linked to the development of obesity. Herein we investigated a library of 53 novel chemicals, generated from a number of polyphenolic natural compounds, on adipogenesis. Strikingly, among the chemicals tested, KMU-3, a derivative of gallic acid, strongly suppressed lipid accumulation during the differentiation of 3T3-L1 preadipocytes into adipocytes. On mechanistic levels, KMU-3 inhibited expressions of CCAAT/enhancer-binding protein-α (C/EBP-α), peroxisome proliferator-activated receptor-γ (PPAR-γ), and fatty acid synthase (FAS) during adipocyte differentiation. Moreover, KMU-3 reduced expressions of adipokines, including retinol binding protein-4 (RBP-4), leptin, and regulated on activation, normal T cell expressed and secreted (RANTES) during adipocyte differentiation. Of further note, KMU-3 rapidly blocked the phosphorylation of signal transducer and activator of transcription-3 (STAT-3) during the early stage of adipogenesis. Importantly, pharmacological inhibition studies revealed that AG490, a JAK-2/STAT-3 inhibitor suppressed adipogenesis and STAT-3 phosphorylation, implying that early blockage of STAT-3 activity is crucial for the KMU-3-mediated anti-adipogenesis. These findings demonstrate firstly that KMU-3 inhibits adipogenesis by down-regulating STAT-3, PPAR-γ, C/EBP-α, and FAS. This work shows that KMU-3 is an inhibitor of adipogenesis and thus may have therapeutic potential against obesity.
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titleIdentification of KMU-3, a novel derivative of gallic acid, as an inhibitor of adipogenesis.
authorPark, Yu-Kyoung ; Lee, Jinho ; Hong, Victor Sukbong ; Choi, Jong-Soon ; Lee, Tae-Yoon ; Jang, Byeong-Churl
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