Beneficial Effect of Taraxacum coreanum Nakai via the Activation of LKB1-AMPK Signaling Pathway on Obesity
Objective. Liver kinase B (LKB) 1 and AMP-activated protein kinase (AMPK) are master regulators and sensors for energy homeostasis. AMPK is mainly activated via phosphorylation of LKB1 under energy stress. Here, we highlighted the antiobesity effect and underlying mechanism of Taraxacum coreanum Nak...
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| creator | Shin, Mi-Rae Kim, Min Ju Park, Hae-Jin Han, Jegeun Roh, Seong-Soo |
| description | Objective. Liver kinase B (LKB) 1 and AMP-activated protein kinase (AMPK) are master regulators and sensors for energy homeostasis. AMPK is mainly activated via phosphorylation of LKB1 under energy stress. Here, we highlighted the antiobesity effect and underlying mechanism of Taraxacum coreanum Nakai (TCN) in connection with LKB1-AMPK signaling pathway. Methods. Male C57BL/6 mice were fed on a high-fat diet (60% kcal fat; HFD) to induce obesity. Simultaneously, they received 100 or 200 mg/kg TCN orally for 5 weeks. We measured the body weight gain and liver weight along with liver histology. Moreover, the changes of factors related to lipid metabolism and β-oxidation were analyzed in the liver, together with blood parameters. Results. The body weights were decreased in mice of the TCN200 group more than those of the HFD control group. Moreover, TCN supplementation lowered serum triglyceride (TG) and total cholesterol (TC) levels, whereas TCN increased HDL-cholesterol level. Liver pathological damage induced by HFD was alleviated with TCN treatment and accompanied with significant reduction in serum AST and ALT activities. In addition, TCN significantly increased the expression of p-AMPK compared with the HFD control group via the activation of LKB1/AMPK signaling pathway. Lipid synthesis gene like ACC was downregulated and factors related to β-oxidation such as carnitine palmitoyl transferase-1 (CPT-1) and uncoupling protein 2 (UCP-2) were upregulated through peroxisome proliferator-activated receptor (PPAR) α activation. Conclusion. Taken together, these data suggest that TCN treatment regulates lipid metabolism via LKB1-AMPK signaling pathway and promotes β-oxidation by PPARα; hence, TCN may have potential remedy in the prevention and treatment of obesity. |
| doi_str_mv | 10.1155/2021/6655599 |
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Liver kinase B (LKB) 1 and AMP-activated protein kinase (AMPK) are master regulators and sensors for energy homeostasis. AMPK is mainly activated via phosphorylation of LKB1 under energy stress. Here, we highlighted the antiobesity effect and underlying mechanism of Taraxacum coreanum Nakai (TCN) in connection with LKB1-AMPK signaling pathway. Methods. Male C57BL/6 mice were fed on a high-fat diet (60% kcal fat; HFD) to induce obesity. Simultaneously, they received 100 or 200 mg/kg TCN orally for 5 weeks. We measured the body weight gain and liver weight along with liver histology. Moreover, the changes of factors related to lipid metabolism and β-oxidation were analyzed in the liver, together with blood parameters. Results. The body weights were decreased in mice of the TCN200 group more than those of the HFD control group. Moreover, TCN supplementation lowered serum triglyceride (TG) and total cholesterol (TC) levels, whereas TCN increased HDL-cholesterol level. Liver pathological damage induced by HFD was alleviated with TCN treatment and accompanied with significant reduction in serum AST and ALT activities. In addition, TCN significantly increased the expression of p-AMPK compared with the HFD control group via the activation of LKB1/AMPK signaling pathway. Lipid synthesis gene like ACC was downregulated and factors related to β-oxidation such as carnitine palmitoyl transferase-1 (CPT-1) and uncoupling protein 2 (UCP-2) were upregulated through peroxisome proliferator-activated receptor (PPAR) α activation. Conclusion. Taken together, these data suggest that TCN treatment regulates lipid metabolism via LKB1-AMPK signaling pathway and promotes β-oxidation by PPARα; hence, TCN may have potential remedy in the prevention and treatment of obesity.</description><identifier>ISSN: 1741-427X</identifier><identifier>EISSN: 1741-4288</identifier><identifier>DOI: 10.1155/2021/6655599</identifier><identifier>PMID: 33531919</identifier><language>eng</language><publisher>LONDON: Hindawi</publisher><subject>AMP ; AMP-activated protein kinase ; Body weight gain ; Carnitine ; Cholesterol ; Diabetes ; Dietary supplements ; Energy ; Energy balance ; Ethanol ; Exercise ; Flavonoids ; Glycerol ; High density lipoprotein ; High fat diet ; Homeostasis ; Integrative & Complementary Medicine ; Kinases ; Life Sciences & Biomedicine ; Lipid metabolism ; Liver ; LKB1 protein ; Metabolism ; Methods ; Mitochondrial uncoupling protein 2 ; Obesity ; Overweight ; Oxidation ; Peroxisome proliferator-activated receptors ; Phosphorylation ; Physical fitness ; Polyclonal antibodies ; Reagents ; Science & Technology ; Signal transduction ; Taraxacum ; Weight control</subject><ispartof>Evidence-based complementary and alternative medicine, 2021, Vol.2021, p.6655599-12, Article 6655599</ispartof><rights>Copyright © 2021 Mi-Rae Shin et al.</rights><rights>Copyright © 2021 Mi-Rae Shin et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2021 Mi-Rae Shin et al. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>7</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000616067800003</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c448t-b38a7320bfe83c73172d3ab1a3755c2e109d70b03dd26acdd9c4e5a86b4676433</citedby><cites>FETCH-LOGICAL-c448t-b38a7320bfe83c73172d3ab1a3755c2e109d70b03dd26acdd9c4e5a86b4676433</cites><orcidid>0000-0002-4283-0809 ; 0000-0002-8912-8267 ; 0000-0002-4162-6849 ; 0000-0001-5901-3242 ; 0000-0002-4365-6988</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7834777/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7834777/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,886,4025,27927,27928,27929,53795,53797</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33531919$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Khanavi, Mahnaz</contributor><contributor>Mahnaz Khanavi</contributor><creatorcontrib>Shin, Mi-Rae</creatorcontrib><creatorcontrib>Kim, Min Ju</creatorcontrib><creatorcontrib>Park, Hae-Jin</creatorcontrib><creatorcontrib>Han, Jegeun</creatorcontrib><creatorcontrib>Roh, Seong-Soo</creatorcontrib><title>Beneficial Effect of Taraxacum coreanum Nakai via the Activation of LKB1-AMPK Signaling Pathway on Obesity</title><title>Evidence-based complementary and alternative medicine</title><addtitle>EVID-BASED COMPL ALT</addtitle><addtitle>Evid Based Complement Alternat Med</addtitle><description>Objective. Liver kinase B (LKB) 1 and AMP-activated protein kinase (AMPK) are master regulators and sensors for energy homeostasis. AMPK is mainly activated via phosphorylation of LKB1 under energy stress. Here, we highlighted the antiobesity effect and underlying mechanism of Taraxacum coreanum Nakai (TCN) in connection with LKB1-AMPK signaling pathway. Methods. Male C57BL/6 mice were fed on a high-fat diet (60% kcal fat; HFD) to induce obesity. Simultaneously, they received 100 or 200 mg/kg TCN orally for 5 weeks. We measured the body weight gain and liver weight along with liver histology. Moreover, the changes of factors related to lipid metabolism and β-oxidation were analyzed in the liver, together with blood parameters. Results. The body weights were decreased in mice of the TCN200 group more than those of the HFD control group. Moreover, TCN supplementation lowered serum triglyceride (TG) and total cholesterol (TC) levels, whereas TCN increased HDL-cholesterol level. Liver pathological damage induced by HFD was alleviated with TCN treatment and accompanied with significant reduction in serum AST and ALT activities. In addition, TCN significantly increased the expression of p-AMPK compared with the HFD control group via the activation of LKB1/AMPK signaling pathway. Lipid synthesis gene like ACC was downregulated and factors related to β-oxidation such as carnitine palmitoyl transferase-1 (CPT-1) and uncoupling protein 2 (UCP-2) were upregulated through peroxisome proliferator-activated receptor (PPAR) α activation. Conclusion. Taken together, these data suggest that TCN treatment regulates lipid metabolism via LKB1-AMPK signaling pathway and promotes β-oxidation by PPARα; hence, TCN may have potential remedy in the prevention and treatment of obesity.</description><subject>AMP</subject><subject>AMP-activated protein kinase</subject><subject>Body weight gain</subject><subject>Carnitine</subject><subject>Cholesterol</subject><subject>Diabetes</subject><subject>Dietary supplements</subject><subject>Energy</subject><subject>Energy balance</subject><subject>Ethanol</subject><subject>Exercise</subject><subject>Flavonoids</subject><subject>Glycerol</subject><subject>High density lipoprotein</subject><subject>High fat diet</subject><subject>Homeostasis</subject><subject>Integrative & Complementary Medicine</subject><subject>Kinases</subject><subject>Life Sciences & Biomedicine</subject><subject>Lipid metabolism</subject><subject>Liver</subject><subject>LKB1 protein</subject><subject>Metabolism</subject><subject>Methods</subject><subject>Mitochondrial uncoupling protein 2</subject><subject>Obesity</subject><subject>Overweight</subject><subject>Oxidation</subject><subject>Peroxisome proliferator-activated receptors</subject><subject>Phosphorylation</subject><subject>Physical fitness</subject><subject>Polyclonal antibodies</subject><subject>Reagents</subject><subject>Science & Technology</subject><subject>Signal transduction</subject><subject>Taraxacum</subject><subject>Weight 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Effect of Taraxacum coreanum Nakai via the Activation of LKB1-AMPK Signaling Pathway on Obesity</title><author>Shin, Mi-Rae ; Kim, Min Ju ; Park, Hae-Jin ; Han, Jegeun ; Roh, Seong-Soo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-b38a7320bfe83c73172d3ab1a3755c2e109d70b03dd26acdd9c4e5a86b4676433</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>AMP</topic><topic>AMP-activated protein kinase</topic><topic>Body weight gain</topic><topic>Carnitine</topic><topic>Cholesterol</topic><topic>Diabetes</topic><topic>Dietary supplements</topic><topic>Energy</topic><topic>Energy balance</topic><topic>Ethanol</topic><topic>Exercise</topic><topic>Flavonoids</topic><topic>Glycerol</topic><topic>High density lipoprotein</topic><topic>High fat diet</topic><topic>Homeostasis</topic><topic>Integrative & Complementary Medicine</topic><topic>Kinases</topic><topic>Life Sciences & Biomedicine</topic><topic>Lipid metabolism</topic><topic>Liver</topic><topic>LKB1 protein</topic><topic>Metabolism</topic><topic>Methods</topic><topic>Mitochondrial uncoupling protein 2</topic><topic>Obesity</topic><topic>Overweight</topic><topic>Oxidation</topic><topic>Peroxisome proliferator-activated receptors</topic><topic>Phosphorylation</topic><topic>Physical fitness</topic><topic>Polyclonal antibodies</topic><topic>Reagents</topic><topic>Science & Technology</topic><topic>Signal transduction</topic><topic>Taraxacum</topic><topic>Weight control</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shin, Mi-Rae</creatorcontrib><creatorcontrib>Kim, Min Ju</creatorcontrib><creatorcontrib>Park, Hae-Jin</creatorcontrib><creatorcontrib>Han, Jegeun</creatorcontrib><creatorcontrib>Roh, Seong-Soo</creatorcontrib><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi 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Signaling Pathway on Obesity</atitle><jtitle>Evidence-based complementary and alternative medicine</jtitle><stitle>EVID-BASED COMPL ALT</stitle><addtitle>Evid Based Complement Alternat Med</addtitle><date>2021</date><risdate>2021</risdate><volume>2021</volume><spage>6655599</spage><epage>12</epage><pages>6655599-12</pages><artnum>6655599</artnum><issn>1741-427X</issn><eissn>1741-4288</eissn><abstract>Objective. Liver kinase B (LKB) 1 and AMP-activated protein kinase (AMPK) are master regulators and sensors for energy homeostasis. AMPK is mainly activated via phosphorylation of LKB1 under energy stress. Here, we highlighted the antiobesity effect and underlying mechanism of Taraxacum coreanum Nakai (TCN) in connection with LKB1-AMPK signaling pathway. Methods. Male C57BL/6 mice were fed on a high-fat diet (60% kcal fat; HFD) to induce obesity. Simultaneously, they received 100 or 200 mg/kg TCN orally for 5 weeks. We measured the body weight gain and liver weight along with liver histology. Moreover, the changes of factors related to lipid metabolism and β-oxidation were analyzed in the liver, together with blood parameters. Results. The body weights were decreased in mice of the TCN200 group more than those of the HFD control group. Moreover, TCN supplementation lowered serum triglyceride (TG) and total cholesterol (TC) levels, whereas TCN increased HDL-cholesterol level. Liver pathological damage induced by HFD was alleviated with TCN treatment and accompanied with significant reduction in serum AST and ALT activities. In addition, TCN significantly increased the expression of p-AMPK compared with the HFD control group via the activation of LKB1/AMPK signaling pathway. Lipid synthesis gene like ACC was downregulated and factors related to β-oxidation such as carnitine palmitoyl transferase-1 (CPT-1) and uncoupling protein 2 (UCP-2) were upregulated through peroxisome proliferator-activated receptor (PPAR) α activation. Conclusion. Taken together, these data suggest that TCN treatment regulates lipid metabolism via LKB1-AMPK signaling pathway and promotes β-oxidation by PPARα; hence, TCN may have potential remedy in the prevention and treatment of obesity.</abstract><cop>LONDON</cop><pub>Hindawi</pub><pmid>33531919</pmid><doi>10.1155/2021/6655599</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-4283-0809</orcidid><orcidid>https://orcid.org/0000-0002-8912-8267</orcidid><orcidid>https://orcid.org/0000-0002-4162-6849</orcidid><orcidid>https://orcid.org/0000-0001-5901-3242</orcidid><orcidid>https://orcid.org/0000-0002-4365-6988</orcidid><oa>free_for_read</oa></addata></record> |
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| source | PubMed Central Open Access; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); PubMed Central; Alma/SFX Local Collection |
| subjects | AMP AMP-activated protein kinase Body weight gain Carnitine Cholesterol Diabetes Dietary supplements Energy Energy balance Ethanol Exercise Flavonoids Glycerol High density lipoprotein High fat diet Homeostasis Integrative & Complementary Medicine Kinases Life Sciences & Biomedicine Lipid metabolism Liver LKB1 protein Metabolism Methods Mitochondrial uncoupling protein 2 Obesity Overweight Oxidation Peroxisome proliferator-activated receptors Phosphorylation Physical fitness Polyclonal antibodies Reagents Science & Technology Signal transduction Taraxacum Weight control |
| title | Beneficial Effect of Taraxacum coreanum Nakai via the Activation of LKB1-AMPK Signaling Pathway on Obesity |
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