Garcinia Cambogia attenuates diet-induced adiposity but exacerbates hepatic collagen accumulation and inflammation

To investigate long-term effects of Garcinia Cambogia (GC), weight-loss supplement, on adiposity and non-alcoholic fatty liver disease in obese mice. Obesity-prone C57BL/6J mice were fed a high-fat diet (HFD, 45 kcal% fat) with or without GC (1%, w/w) for 16 wk. The HFD contained 45 kcal% fat, 20 kc...

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Veröffentlicht in:World journal of gastroenterology : WJG 2013-08, Vol.19 (29), p.4689-4701
Hauptverfasser: Kim, Young-Je, Choi, Myung-Sook, Park, Yong Bok, Kim, Sang Ryong, Lee, Mi-Kyung, Jung, Un Ju
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container_title World journal of gastroenterology : WJG
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creator Kim, Young-Je
Choi, Myung-Sook
Park, Yong Bok
Kim, Sang Ryong
Lee, Mi-Kyung
Jung, Un Ju
description To investigate long-term effects of Garcinia Cambogia (GC), weight-loss supplement, on adiposity and non-alcoholic fatty liver disease in obese mice. Obesity-prone C57BL/6J mice were fed a high-fat diet (HFD, 45 kcal% fat) with or without GC (1%, w/w) for 16 wk. The HFD contained 45 kcal% fat, 20 kcal% protein and 35 kcal% carbohydrate. They were given free access to food and distilled water, and food consumption and body weight were measured daily and weekly, respectively. Data were expressed as the mean ± SE. Statistical analyses were performed using the statistical package for the social science software program. Student's t test was used to assess the differences between the groups. Statistical significance was considered at P < 0.05. There were no significant changes in body weight and food intake between the groups. However, the supplementation of GC significantly lowered visceral fat accumulation and adipocyte size via inhibition of fatty acid synthase activity and its mRNA expression in visceral adipose tissue, along with enhanced enzymatic activity and gene expression involved in adipose fatty acid β-oxidation. Moreover, GC supplementation resulted in significant reductions in glucose intolerance and the plasma resistin level in the HFD-fed mice. However, we first demonstrated that it increased hepatic collagen accumulation, lipid peroxidation and mRNA levels of genes related to oxidative stress (superoxide dismutase and glutathione peroxidase) and inflammatory responses (tumor necrosis factor-α and monocyte chemoattractant protein-1) as well as plasma alanine transaminase and aspartate transaminase levels, although HFD-induced hepatic steatosis was not altered. GC protects against HFD-induced obesity by modulating adipose fatty acid synthesis and β-oxidation but induces hepatic fibrosis, inflammation and oxidative stress.
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Obesity-prone C57BL/6J mice were fed a high-fat diet (HFD, 45 kcal% fat) with or without GC (1%, w/w) for 16 wk. The HFD contained 45 kcal% fat, 20 kcal% protein and 35 kcal% carbohydrate. They were given free access to food and distilled water, and food consumption and body weight were measured daily and weekly, respectively. Data were expressed as the mean ± SE. Statistical analyses were performed using the statistical package for the social science software program. Student's t test was used to assess the differences between the groups. Statistical significance was considered at P &lt; 0.05. There were no significant changes in body weight and food intake between the groups. However, the supplementation of GC significantly lowered visceral fat accumulation and adipocyte size via inhibition of fatty acid synthase activity and its mRNA expression in visceral adipose tissue, along with enhanced enzymatic activity and gene expression involved in adipose fatty acid β-oxidation. Moreover, GC supplementation resulted in significant reductions in glucose intolerance and the plasma resistin level in the HFD-fed mice. However, we first demonstrated that it increased hepatic collagen accumulation, lipid peroxidation and mRNA levels of genes related to oxidative stress (superoxide dismutase and glutathione peroxidase) and inflammatory responses (tumor necrosis factor-α and monocyte chemoattractant protein-1) as well as plasma alanine transaminase and aspartate transaminase levels, although HFD-induced hepatic steatosis was not altered. 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All rights reserved. 2013</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c354t-3593a0bd714396a680ac54966f9afc341b3d34382961ea8d913f0dd916048c2d3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3732841/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3732841/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23922466$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Young-Je</creatorcontrib><creatorcontrib>Choi, Myung-Sook</creatorcontrib><creatorcontrib>Park, Yong Bok</creatorcontrib><creatorcontrib>Kim, Sang Ryong</creatorcontrib><creatorcontrib>Lee, Mi-Kyung</creatorcontrib><creatorcontrib>Jung, Un Ju</creatorcontrib><title>Garcinia Cambogia attenuates diet-induced adiposity but exacerbates hepatic collagen accumulation and inflammation</title><title>World journal of gastroenterology : WJG</title><addtitle>World J Gastroenterol</addtitle><description>To investigate long-term effects of Garcinia Cambogia (GC), weight-loss supplement, on adiposity and non-alcoholic fatty liver disease in obese mice. Obesity-prone C57BL/6J mice were fed a high-fat diet (HFD, 45 kcal% fat) with or without GC (1%, w/w) for 16 wk. The HFD contained 45 kcal% fat, 20 kcal% protein and 35 kcal% carbohydrate. They were given free access to food and distilled water, and food consumption and body weight were measured daily and weekly, respectively. Data were expressed as the mean ± SE. Statistical analyses were performed using the statistical package for the social science software program. Student's t test was used to assess the differences between the groups. Statistical significance was considered at P &lt; 0.05. There were no significant changes in body weight and food intake between the groups. However, the supplementation of GC significantly lowered visceral fat accumulation and adipocyte size via inhibition of fatty acid synthase activity and its mRNA expression in visceral adipose tissue, along with enhanced enzymatic activity and gene expression involved in adipose fatty acid β-oxidation. Moreover, GC supplementation resulted in significant reductions in glucose intolerance and the plasma resistin level in the HFD-fed mice. However, we first demonstrated that it increased hepatic collagen accumulation, lipid peroxidation and mRNA levels of genes related to oxidative stress (superoxide dismutase and glutathione peroxidase) and inflammatory responses (tumor necrosis factor-α and monocyte chemoattractant protein-1) as well as plasma alanine transaminase and aspartate transaminase levels, although HFD-induced hepatic steatosis was not altered. GC protects against HFD-induced obesity by modulating adipose fatty acid synthesis and β-oxidation but induces hepatic fibrosis, inflammation and oxidative stress.</description><subject>Adiposity - drug effects</subject><subject>Animals</subject><subject>Anti-Obesity Agents - toxicity</subject><subject>Blood Glucose - drug effects</subject><subject>Blood Glucose - metabolism</subject><subject>Chemical and Drug Induced Liver Injury - blood</subject><subject>Chemical and Drug Induced Liver Injury - etiology</subject><subject>Chemical and Drug Induced Liver Injury - genetics</subject><subject>Chemical and Drug Induced Liver Injury - immunology</subject><subject>Chemical and Drug Induced Liver Injury - pathology</subject><subject>Collagen - metabolism</subject><subject>Cytokines - blood</subject><subject>Diet, High-Fat</subject><subject>Disease Models, Animal</subject><subject>Fatty Acid Synthase, Type I - antagonists &amp; inhibitors</subject><subject>Fatty Acid Synthase, Type I - genetics</subject><subject>Fatty Acid Synthase, Type I - metabolism</subject><subject>Fatty Liver - blood</subject><subject>Fatty Liver - chemically induced</subject><subject>Fatty Liver - genetics</subject><subject>Fatty Liver - immunology</subject><subject>Fatty Liver - pathology</subject><subject>Garcinia cambogia</subject><subject>Gene Expression Regulation</subject><subject>Glucose Intolerance - blood</subject><subject>Glucose Intolerance - drug therapy</subject><subject>Glucose Intolerance - etiology</subject><subject>Inflammation Mediators - blood</subject><subject>Insulin - blood</subject><subject>Intra-Abdominal Fat - drug effects</subject><subject>Intra-Abdominal Fat - metabolism</subject><subject>Intra-Abdominal Fat - pathology</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Liver Cirrhosis, Experimental - blood</subject><subject>Liver Cirrhosis, Experimental - chemically induced</subject><subject>Liver Cirrhosis, Experimental - genetics</subject><subject>Liver Cirrhosis, Experimental - immunology</subject><subject>Liver Cirrhosis, Experimental - pathology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Obese</subject><subject>Non-alcoholic Fatty Liver Disease</subject><subject>Obesity - blood</subject><subject>Obesity - drug therapy</subject><subject>Obesity - etiology</subject><subject>Obesity - genetics</subject><subject>Obesity - immunology</subject><subject>Obesity - pathology</subject><subject>Original</subject><subject>Oxidative Stress - drug effects</subject><subject>Phytotherapy</subject><subject>Plant Extracts - toxicity</subject><subject>Plants, Medicinal</subject><subject>Resistin - blood</subject><subject>RNA, Messenger - metabolism</subject><subject>Time Factors</subject><issn>1007-9327</issn><issn>2219-2840</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkFtLxDAQhYMo7rr67pP0D7QmmTRtXgRZvIHgiz6HaZLWLL0sberl3xtdFX2amTNzzsBHyCmjGRSiPH_dNNkLU5nnKhOyVHtkyTlTKS8F3SdLRmmRKuDFghxN04ZSDpDzQ7LgoDgXUi7JeIOj8b3HZI1dNTSxwRBcP2NwU2K9C6nv7WycTdD67TD58J5Uc0jcGxo3Vl9nz26LwZvEDG2LjesTNGbu5jaKQxx6m_i-brHrvoRjclBjO7mT77oiT9dXj-vb9P7h5m59eZ8ayEVIIVeAtLIFE6AkypKiyYWSslZYGxCsAgsCSq4kc1haxaCmNhZJRWm4hRW52OVu56pz1rg-jNjq7eg7HN_1gF7_3_T-WTfDi4YCIkAWA-guwIzDNI2u_vUyqj_568hfR_468tef_KPl7O_PX8MPcPgAKbuGUw</recordid><startdate>20130807</startdate><enddate>20130807</enddate><creator>Kim, Young-Je</creator><creator>Choi, Myung-Sook</creator><creator>Park, Yong Bok</creator><creator>Kim, Sang Ryong</creator><creator>Lee, Mi-Kyung</creator><creator>Jung, Un Ju</creator><general>Baishideng Publishing Group Co., Limited</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>5PM</scope></search><sort><creationdate>20130807</creationdate><title>Garcinia Cambogia attenuates diet-induced adiposity but exacerbates hepatic collagen accumulation and inflammation</title><author>Kim, Young-Je ; Choi, Myung-Sook ; Park, Yong Bok ; Kim, Sang Ryong ; Lee, Mi-Kyung ; Jung, Un Ju</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c354t-3593a0bd714396a680ac54966f9afc341b3d34382961ea8d913f0dd916048c2d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adiposity - drug effects</topic><topic>Animals</topic><topic>Anti-Obesity Agents - toxicity</topic><topic>Blood Glucose - drug effects</topic><topic>Blood Glucose - metabolism</topic><topic>Chemical and Drug Induced Liver Injury - blood</topic><topic>Chemical and Drug Induced Liver Injury - etiology</topic><topic>Chemical and Drug Induced Liver Injury - genetics</topic><topic>Chemical and Drug Induced Liver Injury - immunology</topic><topic>Chemical and Drug Induced Liver Injury - pathology</topic><topic>Collagen - metabolism</topic><topic>Cytokines - blood</topic><topic>Diet, High-Fat</topic><topic>Disease Models, Animal</topic><topic>Fatty Acid Synthase, Type I - antagonists &amp; inhibitors</topic><topic>Fatty Acid Synthase, Type I - genetics</topic><topic>Fatty Acid Synthase, Type I - metabolism</topic><topic>Fatty Liver - blood</topic><topic>Fatty Liver - chemically induced</topic><topic>Fatty Liver - genetics</topic><topic>Fatty Liver - immunology</topic><topic>Fatty Liver - pathology</topic><topic>Garcinia cambogia</topic><topic>Gene Expression Regulation</topic><topic>Glucose Intolerance - blood</topic><topic>Glucose Intolerance - drug therapy</topic><topic>Glucose Intolerance - etiology</topic><topic>Inflammation Mediators - blood</topic><topic>Insulin - blood</topic><topic>Intra-Abdominal Fat - drug effects</topic><topic>Intra-Abdominal Fat - metabolism</topic><topic>Intra-Abdominal Fat - pathology</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Liver - drug effects</topic><topic>Liver - metabolism</topic><topic>Liver - pathology</topic><topic>Liver Cirrhosis, Experimental - blood</topic><topic>Liver Cirrhosis, Experimental - chemically induced</topic><topic>Liver Cirrhosis, Experimental - genetics</topic><topic>Liver Cirrhosis, Experimental - immunology</topic><topic>Liver Cirrhosis, Experimental - pathology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Obese</topic><topic>Non-alcoholic Fatty Liver Disease</topic><topic>Obesity - blood</topic><topic>Obesity - drug therapy</topic><topic>Obesity - etiology</topic><topic>Obesity - genetics</topic><topic>Obesity - immunology</topic><topic>Obesity - pathology</topic><topic>Original</topic><topic>Oxidative Stress - drug effects</topic><topic>Phytotherapy</topic><topic>Plant Extracts - toxicity</topic><topic>Plants, Medicinal</topic><topic>Resistin - blood</topic><topic>RNA, Messenger - metabolism</topic><topic>Time Factors</topic><toplevel>online_resources</toplevel><creatorcontrib>Kim, Young-Je</creatorcontrib><creatorcontrib>Choi, Myung-Sook</creatorcontrib><creatorcontrib>Park, Yong Bok</creatorcontrib><creatorcontrib>Kim, Sang Ryong</creatorcontrib><creatorcontrib>Lee, Mi-Kyung</creatorcontrib><creatorcontrib>Jung, Un Ju</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>World journal of gastroenterology : WJG</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Young-Je</au><au>Choi, Myung-Sook</au><au>Park, Yong Bok</au><au>Kim, Sang Ryong</au><au>Lee, Mi-Kyung</au><au>Jung, Un Ju</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Garcinia Cambogia attenuates diet-induced adiposity but exacerbates hepatic collagen accumulation and inflammation</atitle><jtitle>World journal of gastroenterology : WJG</jtitle><addtitle>World J Gastroenterol</addtitle><date>2013-08-07</date><risdate>2013</risdate><volume>19</volume><issue>29</issue><spage>4689</spage><epage>4701</epage><pages>4689-4701</pages><issn>1007-9327</issn><eissn>2219-2840</eissn><abstract>To investigate long-term effects of Garcinia Cambogia (GC), weight-loss supplement, on adiposity and non-alcoholic fatty liver disease in obese mice. Obesity-prone C57BL/6J mice were fed a high-fat diet (HFD, 45 kcal% fat) with or without GC (1%, w/w) for 16 wk. The HFD contained 45 kcal% fat, 20 kcal% protein and 35 kcal% carbohydrate. They were given free access to food and distilled water, and food consumption and body weight were measured daily and weekly, respectively. Data were expressed as the mean ± SE. Statistical analyses were performed using the statistical package for the social science software program. Student's t test was used to assess the differences between the groups. Statistical significance was considered at P &lt; 0.05. There were no significant changes in body weight and food intake between the groups. However, the supplementation of GC significantly lowered visceral fat accumulation and adipocyte size via inhibition of fatty acid synthase activity and its mRNA expression in visceral adipose tissue, along with enhanced enzymatic activity and gene expression involved in adipose fatty acid β-oxidation. Moreover, GC supplementation resulted in significant reductions in glucose intolerance and the plasma resistin level in the HFD-fed mice. However, we first demonstrated that it increased hepatic collagen accumulation, lipid peroxidation and mRNA levels of genes related to oxidative stress (superoxide dismutase and glutathione peroxidase) and inflammatory responses (tumor necrosis factor-α and monocyte chemoattractant protein-1) as well as plasma alanine transaminase and aspartate transaminase levels, although HFD-induced hepatic steatosis was not altered. GC protects against HFD-induced obesity by modulating adipose fatty acid synthesis and β-oxidation but induces hepatic fibrosis, inflammation and oxidative stress.</abstract><cop>United States</cop><pub>Baishideng Publishing Group Co., Limited</pub><pmid>23922466</pmid><doi>10.3748/wjg.v19.i29.4689</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record>
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subjects Adiposity - drug effects
Animals
Anti-Obesity Agents - toxicity
Blood Glucose - drug effects
Blood Glucose - metabolism
Chemical and Drug Induced Liver Injury - blood
Chemical and Drug Induced Liver Injury - etiology
Chemical and Drug Induced Liver Injury - genetics
Chemical and Drug Induced Liver Injury - immunology
Chemical and Drug Induced Liver Injury - pathology
Collagen - metabolism
Cytokines - blood
Diet, High-Fat
Disease Models, Animal
Fatty Acid Synthase, Type I - antagonists & inhibitors
Fatty Acid Synthase, Type I - genetics
Fatty Acid Synthase, Type I - metabolism
Fatty Liver - blood
Fatty Liver - chemically induced
Fatty Liver - genetics
Fatty Liver - immunology
Fatty Liver - pathology
Garcinia cambogia
Gene Expression Regulation
Glucose Intolerance - blood
Glucose Intolerance - drug therapy
Glucose Intolerance - etiology
Inflammation Mediators - blood
Insulin - blood
Intra-Abdominal Fat - drug effects
Intra-Abdominal Fat - metabolism
Intra-Abdominal Fat - pathology
Lipid Peroxidation - drug effects
Liver - drug effects
Liver - metabolism
Liver - pathology
Liver Cirrhosis, Experimental - blood
Liver Cirrhosis, Experimental - chemically induced
Liver Cirrhosis, Experimental - genetics
Liver Cirrhosis, Experimental - immunology
Liver Cirrhosis, Experimental - pathology
Male
Mice
Mice, Inbred C57BL
Mice, Obese
Non-alcoholic Fatty Liver Disease
Obesity - blood
Obesity - drug therapy
Obesity - etiology
Obesity - genetics
Obesity - immunology
Obesity - pathology
Original
Oxidative Stress - drug effects
Phytotherapy
Plant Extracts - toxicity
Plants, Medicinal
Resistin - blood
RNA, Messenger - metabolism
Time Factors
title Garcinia Cambogia attenuates diet-induced adiposity but exacerbates hepatic collagen accumulation and inflammation
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