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<!DOCTYPE ArticleSet PUBLIC "-//NLM//DTD PubMed 2.0//EN" "http://www.ncbi.nlm.nih.gov:80/entrez/query/static/PubMed.dtd">
<ArticleSet>
<Article>
<Journal>
<PublisherName>Science and Education Publishing</PublisherName>
<JournalTitle>Journal of Food and Nutrition Research</JournalTitle>
<Issn>2333-1240</Issn>
<Volume>4</Volume>
<Issue>7</Issue>
<PubDate PubStatus="epublish">
<Year>2016</Year>
<Month>8</Month>
<Day>2</Day>
</PubDate>
</Journal>
<ArticleTitle>Altered Gelidium elegans Extract-stimulated Beige-like Phenotype Attenuates Adipogenesis in 3T3-L1 Cells</ArticleTitle>
<FirstPage>448</FirstPage>
<LastPage>453</LastPage>
<Language>EN</Language>
<AuthorList>
<Author>
<FirstName>Jia</FirstName>
<LastName>Choi</LastName>
</Author>
<Author>
<FirstName>Kui-Jin</FirstName>
<LastName>Kim</LastName>
</Author>
<Author>
<FirstName>Eun-Jeong</FirstName>
<LastName>Koh</LastName>
</Author>
<Author>
<FirstName>Boo-Yong</FirstName>
<LastName>Lee</LastName>
<Affiliation>Department of Food Science and Biotechnology, College of Life Science, CHA University, Seongnam, Kyeonggi 463-400, Republic of Korea</Affiliation>
</Author>

</AuthorList>
<ArticleIdList>
<ArticleId IdType="pii">JFNR2016476</ArticleId>
<ArticleId IdType="doi">10.12691/jfnr-4-7-6</ArticleId>
</ArticleIdList>
<History>
<PubDate PubStatus="received">
<Year>2016</Year>
<Month>4</Month>
<Day>12</Day>
</PubDate>
<PubDate PubStatus="revised">
<Year>2016</Year>
<Month>5</Month>
<Day>15</Day>
</PubDate>
<PubDate PubStatus="accepted">
<Year>2016</Year>
<Month>7</Month>
<Day>31</Day>
</PubDate>
</History>
<Abstract>Previously, we showed that Gelidium elegans extract (GE) suppresses oxidative stress and lipid accumulation. However, the molecular mechanism underlying the anti-adipogenic ability of GE is still unclear. The levels of adipogenesis markers and triglyceride synthesis enzymes were measured by western blot. To evaluate the lipid accumulation in 3T3-L1 cells, oil red o staining was performed. We investigated whether GE induces lipolysis by measuring adipocyte triglyceride lipase (ATGL) during adipocyte differentiation. We also examined the expression of beige cell-associated genes and the production of carbon dioxide in 3T3-L1 cells. We showed that GE increased the protein expression of CAAT/enhancer binding protein (C/EBP) homologous protein 10 and inhibited the expression of C/EBPβ. GE discouraged triglyceride synthesis via deregulation of lysophosphatidic acid acyltransferase-θ (LPAATθ) and diacylglycerolacyltransferase 1 (DGAT1) during late-stage adipogenesis in 3T3-L1 cells. GE also dramatically increased ATGL in 3T3-L1 cells. Finally, in 3T3-L1 cells treated with GE, markers of beige adipocytes such as PRDM16 and UCP1 were upregulated, and large amounts of carbon dioxide were produced. These data indicate that GE suppresses adipogenesis by stimulating a beige-like phenotype in 3T3-L1 cells.</Abstract>
</Article>
</ArticleSet>
