Ginsenoside Rh1 Ameliorates High Fat Diet-Induced Obesity in Mice by Inhibiting Adipocyte Differentiation
Ginseng (the root of Panax ginseng C. A. MEYER), which contains protopanaxadiols and protopanaxatriols as its main constituents, has been used for many disorders, such as cancer, diabetes, inflammation, and hyperlipidemia. Of these ginsenosides, protopanaxadiol ginsenoside Rh2 alone is reported to i...
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| Veröffentlicht in: | Biological & pharmaceutical bulletin 2013/01/01, Vol.36(1), pp.102-107 |
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| description | Ginseng (the root of Panax ginseng C. A. MEYER), which contains protopanaxadiols and protopanaxatriols as its main constituents, has been used for many disorders, such as cancer, diabetes, inflammation, and hyperlipidemia. Of these ginsenosides, protopanaxadiol ginsenoside Rh2 alone is reported to inhibit adipogenesis in 3T3-L1 in vitro. Therefore, we investigated the effect of protopanaxatriol ginsenoside Rh1 on adipogenesis in 3T3-L1 cells and high fat diet-induced obesity (DIO) mice. Treatment with ginsenoside Rh1 inhibited adipogenesis, as evidenced by Oil red O staining and lipid droplet extraction assay. Reverse transcription-polymerase chain reaction (RT-PCR) analysis revealed that ginsenoside Rh1 decreased the expressions of peroxisome proliferator-activated receptor (PPAR)-γ, CCAAT/enhancer-binding protein (C/EBP)-α, fatty acid synthase, and adipocyte fatty acid-binding protein. Oral administration of ginsenoside Rh1 (20 mg/kg) suppressed body and epididymal fat weight gains and plasma triglyceride level in DIO mice. Ginsenoside Rh1 also inhibited the expressions of PPAR-γ, C/EBP-α, fatty acid synthase, adipocyte fatty acid-binding protein, as well as F4/80, CD68, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β in DIO mice by real time PCR analysis. Based on these findings, ginsenoside Rh1 may ameliorate obesity, by inhibiting adipocyte differentiation and inflammation. |
| doi_str_mv | 10.1248/bpb.b12-00558 |
| format | Article |
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A. MEYER), which contains protopanaxadiols and protopanaxatriols as its main constituents, has been used for many disorders, such as cancer, diabetes, inflammation, and hyperlipidemia. Of these ginsenosides, protopanaxadiol ginsenoside Rh2 alone is reported to inhibit adipogenesis in 3T3-L1 in vitro. Therefore, we investigated the effect of protopanaxatriol ginsenoside Rh1 on adipogenesis in 3T3-L1 cells and high fat diet-induced obesity (DIO) mice. Treatment with ginsenoside Rh1 inhibited adipogenesis, as evidenced by Oil red O staining and lipid droplet extraction assay. Reverse transcription-polymerase chain reaction (RT-PCR) analysis revealed that ginsenoside Rh1 decreased the expressions of peroxisome proliferator-activated receptor (PPAR)-γ, CCAAT/enhancer-binding protein (C/EBP)-α, fatty acid synthase, and adipocyte fatty acid-binding protein. Oral administration of ginsenoside Rh1 (20 mg/kg) suppressed body and epididymal fat weight gains and plasma triglyceride level in DIO mice. Ginsenoside Rh1 also inhibited the expressions of PPAR-γ, C/EBP-α, fatty acid synthase, adipocyte fatty acid-binding protein, as well as F4/80, CD68, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β in DIO mice by real time PCR analysis. Based on these findings, ginsenoside Rh1 may ameliorate obesity, by inhibiting adipocyte differentiation and inflammation.</description><identifier>ISSN: 0918-6158</identifier><identifier>EISSN: 1347-5215</identifier><identifier>DOI: 10.1248/bpb.b12-00558</identifier><identifier>PMID: 23302642</identifier><language>eng</language><publisher>Japan: The Pharmaceutical Society of Japan</publisher><subject>3T3-L1 Cells ; Adipocytes - cytology ; Adipocytes - drug effects ; Adipocytes - metabolism ; adipogenesis ; Animals ; Anti-Obesity Agents - pharmacology ; Anti-Obesity Agents - therapeutic use ; CCAAT-Enhancer-Binding Protein-alpha - genetics ; Cell Differentiation - drug effects ; Cholesterol - blood ; Cytokines - metabolism ; Diet, High-Fat ; Epididymis - drug effects ; Epididymis - metabolism ; Fatty Acid Synthases - genetics ; Fatty Acid-Binding Proteins - genetics ; ginsenoside Rh1 ; Ginsenosides - pharmacology ; Ginsenosides - therapeutic use ; Male ; Mice ; Mice, Inbred C57BL ; obesity ; Obesity - drug therapy ; Obesity - metabolism ; Panax ginseng ; PPAR gamma - genetics ; Triglycerides - blood</subject><ispartof>Biological and Pharmaceutical Bulletin, 2013/01/01, Vol.36(1), pp.102-107</ispartof><rights>2013 The Pharmaceutical Society of Japan</rights><rights>Copyright Japan Science and Technology Agency 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c567t-83db648aaec689ab00773c97dd3a7dc3e5fd79ceb9a749f43c5f24dac4f4ac593</citedby><cites>FETCH-LOGICAL-c567t-83db648aaec689ab00773c97dd3a7dc3e5fd79ceb9a749f43c5f24dac4f4ac593</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1881,4022,27922,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23302642$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gu, Wan</creatorcontrib><creatorcontrib>Kim, Kyung-Ah</creatorcontrib><creatorcontrib>Kim, Dong-Hyun</creatorcontrib><title>Ginsenoside Rh1 Ameliorates High Fat Diet-Induced Obesity in Mice by Inhibiting Adipocyte Differentiation</title><title>Biological & pharmaceutical bulletin</title><addtitle>Biol Pharm Bull</addtitle><description>Ginseng (the root of Panax ginseng C. A. MEYER), which contains protopanaxadiols and protopanaxatriols as its main constituents, has been used for many disorders, such as cancer, diabetes, inflammation, and hyperlipidemia. Of these ginsenosides, protopanaxadiol ginsenoside Rh2 alone is reported to inhibit adipogenesis in 3T3-L1 in vitro. Therefore, we investigated the effect of protopanaxatriol ginsenoside Rh1 on adipogenesis in 3T3-L1 cells and high fat diet-induced obesity (DIO) mice. Treatment with ginsenoside Rh1 inhibited adipogenesis, as evidenced by Oil red O staining and lipid droplet extraction assay. Reverse transcription-polymerase chain reaction (RT-PCR) analysis revealed that ginsenoside Rh1 decreased the expressions of peroxisome proliferator-activated receptor (PPAR)-γ, CCAAT/enhancer-binding protein (C/EBP)-α, fatty acid synthase, and adipocyte fatty acid-binding protein. Oral administration of ginsenoside Rh1 (20 mg/kg) suppressed body and epididymal fat weight gains and plasma triglyceride level in DIO mice. Ginsenoside Rh1 also inhibited the expressions of PPAR-γ, C/EBP-α, fatty acid synthase, adipocyte fatty acid-binding protein, as well as F4/80, CD68, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β in DIO mice by real time PCR analysis. Based on these findings, ginsenoside Rh1 may ameliorate obesity, by inhibiting adipocyte differentiation and inflammation.</description><subject>3T3-L1 Cells</subject><subject>Adipocytes - cytology</subject><subject>Adipocytes - drug effects</subject><subject>Adipocytes - metabolism</subject><subject>adipogenesis</subject><subject>Animals</subject><subject>Anti-Obesity Agents - pharmacology</subject><subject>Anti-Obesity Agents - therapeutic use</subject><subject>CCAAT-Enhancer-Binding Protein-alpha - genetics</subject><subject>Cell Differentiation - drug effects</subject><subject>Cholesterol - blood</subject><subject>Cytokines - metabolism</subject><subject>Diet, High-Fat</subject><subject>Epididymis - drug effects</subject><subject>Epididymis - metabolism</subject><subject>Fatty Acid Synthases - genetics</subject><subject>Fatty Acid-Binding Proteins - genetics</subject><subject>ginsenoside Rh1</subject><subject>Ginsenosides - pharmacology</subject><subject>Ginsenosides - therapeutic use</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>obesity</subject><subject>Obesity - drug therapy</subject><subject>Obesity - metabolism</subject><subject>Panax ginseng</subject><subject>PPAR gamma - genetics</subject><subject>Triglycerides - blood</subject><issn>0918-6158</issn><issn>1347-5215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc1vEzEQxS0EoiFw5IosceGyxV-79h6jQNtIrSohOFv-mE0cbbzB9h7y3-M2JYdeZg7zmzdP8xD6TMk1ZUJ9t0d7bSlrCGlb9QYtKBeyaRlt36IF6alqOtqqK_Qh5z0hRBLG36MrxjlhnWALFG5DzBCnHDzgXzuKVwcYw5RMgYzvwnaHb0zBPwKUZhP97MDjRws5lBMOET8EB9ie8Cbugg0lxC1e-XCc3KlAXRoGSBBLMCVM8SN6N5gxw6eXvkR_bn7-Xt8194-3m_XqvnFtJ0ujuLedUMaA61RvbPUsueul99xI7zi0g5e9A9sbKfpBcNcOTHjjxCCMa3u-RN_Ousc0_Z0hF30I2cE4mgjTnDVlknPVd4JX9OsrdD_NKVZ3mgqpCFWqHl-i5ky5NOWcYNDHFA4mnTQl-ikDXTPQNQP9nEHlv7yozvYA_kL_f3oF1mdgn4vZwgUwqQQ3wrMc7zR9KhfZy9TtTNIQ-T9PzZqe</recordid><startdate>20130101</startdate><enddate>20130101</enddate><creator>Gu, Wan</creator><creator>Kim, Kyung-Ah</creator><creator>Kim, Dong-Hyun</creator><general>The Pharmaceutical Society of Japan</general><general>Japan Science and Technology Agency</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20130101</creationdate><title>Ginsenoside Rh1 Ameliorates High Fat Diet-Induced Obesity in Mice by Inhibiting Adipocyte Differentiation</title><author>Gu, Wan ; Kim, Kyung-Ah ; Kim, Dong-Hyun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c567t-83db648aaec689ab00773c97dd3a7dc3e5fd79ceb9a749f43c5f24dac4f4ac593</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>3T3-L1 Cells</topic><topic>Adipocytes - cytology</topic><topic>Adipocytes - drug effects</topic><topic>Adipocytes - metabolism</topic><topic>adipogenesis</topic><topic>Animals</topic><topic>Anti-Obesity Agents - pharmacology</topic><topic>Anti-Obesity Agents - therapeutic use</topic><topic>CCAAT-Enhancer-Binding Protein-alpha - genetics</topic><topic>Cell Differentiation - drug effects</topic><topic>Cholesterol - blood</topic><topic>Cytokines - metabolism</topic><topic>Diet, High-Fat</topic><topic>Epididymis - drug effects</topic><topic>Epididymis - metabolism</topic><topic>Fatty Acid Synthases - genetics</topic><topic>Fatty Acid-Binding Proteins - genetics</topic><topic>ginsenoside Rh1</topic><topic>Ginsenosides - pharmacology</topic><topic>Ginsenosides - therapeutic use</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>obesity</topic><topic>Obesity - drug therapy</topic><topic>Obesity - metabolism</topic><topic>Panax ginseng</topic><topic>PPAR gamma - genetics</topic><topic>Triglycerides - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gu, Wan</creatorcontrib><creatorcontrib>Kim, Kyung-Ah</creatorcontrib><creatorcontrib>Kim, Dong-Hyun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biological & pharmaceutical bulletin</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gu, Wan</au><au>Kim, Kyung-Ah</au><au>Kim, Dong-Hyun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ginsenoside Rh1 Ameliorates High Fat Diet-Induced Obesity in Mice by Inhibiting Adipocyte Differentiation</atitle><jtitle>Biological & pharmaceutical bulletin</jtitle><addtitle>Biol Pharm Bull</addtitle><date>2013-01-01</date><risdate>2013</risdate><volume>36</volume><issue>1</issue><spage>102</spage><epage>107</epage><pages>102-107</pages><issn>0918-6158</issn><eissn>1347-5215</eissn><abstract>Ginseng (the root of Panax ginseng C. A. MEYER), which contains protopanaxadiols and protopanaxatriols as its main constituents, has been used for many disorders, such as cancer, diabetes, inflammation, and hyperlipidemia. Of these ginsenosides, protopanaxadiol ginsenoside Rh2 alone is reported to inhibit adipogenesis in 3T3-L1 in vitro. Therefore, we investigated the effect of protopanaxatriol ginsenoside Rh1 on adipogenesis in 3T3-L1 cells and high fat diet-induced obesity (DIO) mice. Treatment with ginsenoside Rh1 inhibited adipogenesis, as evidenced by Oil red O staining and lipid droplet extraction assay. Reverse transcription-polymerase chain reaction (RT-PCR) analysis revealed that ginsenoside Rh1 decreased the expressions of peroxisome proliferator-activated receptor (PPAR)-γ, CCAAT/enhancer-binding protein (C/EBP)-α, fatty acid synthase, and adipocyte fatty acid-binding protein. Oral administration of ginsenoside Rh1 (20 mg/kg) suppressed body and epididymal fat weight gains and plasma triglyceride level in DIO mice. Ginsenoside Rh1 also inhibited the expressions of PPAR-γ, C/EBP-α, fatty acid synthase, adipocyte fatty acid-binding protein, as well as F4/80, CD68, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β in DIO mice by real time PCR analysis. Based on these findings, ginsenoside Rh1 may ameliorate obesity, by inhibiting adipocyte differentiation and inflammation.</abstract><cop>Japan</cop><pub>The Pharmaceutical Society of Japan</pub><pmid>23302642</pmid><doi>10.1248/bpb.b12-00558</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; J-STAGE (Japan Science & Technology Information Aggregator, Electronic) Freely Available Titles - Japanese; EZB-FREE-00999 freely available EZB journals; Free Full-Text Journals in Chemistry |
| subjects | 3T3-L1 Cells Adipocytes - cytology Adipocytes - drug effects Adipocytes - metabolism adipogenesis Animals Anti-Obesity Agents - pharmacology Anti-Obesity Agents - therapeutic use CCAAT-Enhancer-Binding Protein-alpha - genetics Cell Differentiation - drug effects Cholesterol - blood Cytokines - metabolism Diet, High-Fat Epididymis - drug effects Epididymis - metabolism Fatty Acid Synthases - genetics Fatty Acid-Binding Proteins - genetics ginsenoside Rh1 Ginsenosides - pharmacology Ginsenosides - therapeutic use Male Mice Mice, Inbred C57BL obesity Obesity - drug therapy Obesity - metabolism Panax ginseng PPAR gamma - genetics Triglycerides - blood |
| title | Ginsenoside Rh1 Ameliorates High Fat Diet-Induced Obesity in Mice by Inhibiting Adipocyte Differentiation |
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