Glucose uptake through translocation and activation of GLUT4 in PI3K/Akt signaling pathway by asiatic acid in diabetic rats
In this study, we examined the in vivo effect and the mechanism of asiatic acid (AA) on glucose uptake in an insulin target skeletal muscle. Diabetic rats showed significantly increased levels of plasma glucose, thiobarbituric acid reactive substances, and lipid hydroperoxides, decreased levels of i...
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| Veröffentlicht in: | Human & experimental toxicology 2015-09, Vol.34 (9), p.884-893 |
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| creator | Ramachandran, V Saravanan, R |
| description | In this study, we examined the in vivo effect and the mechanism of asiatic acid (AA) on glucose uptake in an insulin target skeletal muscle. Diabetic rats showed significantly increased levels of plasma glucose, thiobarbituric acid reactive substances, and lipid hydroperoxides, decreased levels of insulin and antioxidants, and impairment in insulin-signaling proteins such as insulin receptor (IR), insulin receptor substrate (IRS)-1/2, phosphoinositide 3-kinase (PI3K), Akt, and glucose transporter 4 (GLUT4) proteins. Oral treatment with AA (20 mg/kg body weight) showed near-normalized levels of plasma glucose, lipid peroxidation products, and antioxidants and improved insulin, IR, IRS-1/2, PI3K, Akt, and GLUT4 proteins. These findings suggest that AA improves glucose response by increasing GLUT4 in skeletal muscle through Akt and antioxidant defense in plasma and it also improves glucose homeostasis. |
| doi_str_mv | 10.1177/0960327114561663 |
| format | Article |
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Diabetic rats showed significantly increased levels of plasma glucose, thiobarbituric acid reactive substances, and lipid hydroperoxides, decreased levels of insulin and antioxidants, and impairment in insulin-signaling proteins such as insulin receptor (IR), insulin receptor substrate (IRS)-1/2, phosphoinositide 3-kinase (PI3K), Akt, and glucose transporter 4 (GLUT4) proteins. Oral treatment with AA (20 mg/kg body weight) showed near-normalized levels of plasma glucose, lipid peroxidation products, and antioxidants and improved insulin, IR, IRS-1/2, PI3K, Akt, and GLUT4 proteins. These findings suggest that AA improves glucose response by increasing GLUT4 in skeletal muscle through Akt and antioxidant defense in plasma and it also improves glucose homeostasis.</description><identifier>ISSN: 0960-3271</identifier><identifier>EISSN: 1477-0903</identifier><identifier>DOI: 10.1177/0960327114561663</identifier><identifier>PMID: 26286522</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Acids ; Animals ; Antioxidants - metabolism ; Diabetes ; Diabetes Mellitus, Experimental - blood ; Diabetes Mellitus, Experimental - metabolism ; Glucose ; Glucose - metabolism ; Glucose Transporter Type 4 - drug effects ; Glucose Transporter Type 4 - metabolism ; Insulin ; Insulin - blood ; Lipid Peroxidation - drug effects ; Male ; Oncogene Protein v-akt - drug effects ; Oncogene Protein v-akt - metabolism ; Pentacyclic Triterpenes - pharmacology ; Phosphatidylinositol 3-Kinases - drug effects ; Phosphatidylinositol 3-Kinases - metabolism ; Rats ; Rats, Wistar ; Receptor, Insulin - biosynthesis ; Rodents ; Signal Transduction - drug effects ; Studies ; Thiobarbituric Acid Reactive Substances - metabolism</subject><ispartof>Human & experimental toxicology, 2015-09, Vol.34 (9), p.884-893</ispartof><rights>The Author(s) 2014</rights><rights>The Author(s) 2014.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c473t-f71879f2545e30dc49676f9e2548da992a73713523e06f3aa4a2de29234615923</citedby><cites>FETCH-LOGICAL-c473t-f71879f2545e30dc49676f9e2548da992a73713523e06f3aa4a2de29234615923</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/0960327114561663$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/0960327114561663$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,780,784,21964,27851,27922,27923,44943,45331</link.rule.ids><linktorsrc>$$Uhttps://journals.sagepub.com/doi/full/10.1177/0960327114561663?utm_source=summon&utm_medium=discovery-provider$$EView_record_in_SAGE_Publications$$FView_record_in_$$GSAGE_Publications</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26286522$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ramachandran, V</creatorcontrib><creatorcontrib>Saravanan, R</creatorcontrib><title>Glucose uptake through translocation and activation of GLUT4 in PI3K/Akt signaling pathway by asiatic acid in diabetic rats</title><title>Human & experimental toxicology</title><addtitle>Hum Exp Toxicol</addtitle><description>In this study, we examined the in vivo effect and the mechanism of asiatic acid (AA) on glucose uptake in an insulin target skeletal muscle. Diabetic rats showed significantly increased levels of plasma glucose, thiobarbituric acid reactive substances, and lipid hydroperoxides, decreased levels of insulin and antioxidants, and impairment in insulin-signaling proteins such as insulin receptor (IR), insulin receptor substrate (IRS)-1/2, phosphoinositide 3-kinase (PI3K), Akt, and glucose transporter 4 (GLUT4) proteins. Oral treatment with AA (20 mg/kg body weight) showed near-normalized levels of plasma glucose, lipid peroxidation products, and antioxidants and improved insulin, IR, IRS-1/2, PI3K, Akt, and GLUT4 proteins. These findings suggest that AA improves glucose response by increasing GLUT4 in skeletal muscle through Akt and antioxidant defense in plasma and it also improves glucose homeostasis.</description><subject>Acids</subject><subject>Animals</subject><subject>Antioxidants - metabolism</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Experimental - blood</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Glucose Transporter Type 4 - drug effects</subject><subject>Glucose Transporter Type 4 - metabolism</subject><subject>Insulin</subject><subject>Insulin - blood</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Male</subject><subject>Oncogene Protein v-akt - drug effects</subject><subject>Oncogene Protein v-akt - metabolism</subject><subject>Pentacyclic Triterpenes - pharmacology</subject><subject>Phosphatidylinositol 3-Kinases - drug effects</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptor, Insulin - biosynthesis</subject><subject>Rodents</subject><subject>Signal Transduction - drug effects</subject><subject>Studies</subject><subject>Thiobarbituric Acid Reactive Substances - metabolism</subject><issn>0960-3271</issn><issn>1477-0903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kM1Lw0AQxRdRbK3ePcmC59j9yO5mj0W0Fgt6aM9hmmza7UdSdzdK8Z83IVVE8DTMzO-9GR5C15TcUarUkGhJOFOUxkJSKfkJ6tNYqYhowk9Rv11H7b6HLrxfE0KkFvQc9ZhkiRSM9dHneFtnlTe43gfYGBxWrqqXKxwclH5bZRBsVWIocwxZsO9dWxV4PJ3PYmxL_Drhz8PRJmBvlyVsbbnEewirDzjgxQGDt40ka8Q2b-ncwsK0AwfBX6KzArbeXB3rAM0fH2b3T9H0ZTy5H02jLFY8RIWiidIFE7EwnORZrKWShTbNIMlBawaKK8oF44bIggPEwHLDNOOxpKIpA3Tb-e5d9VYbH9J1VbvmWZ9SRYUSQiVJQ5GOylzlvTNFund2B-6QUpK2aad_024kN0fjerEz-Y_gO94GiDrAw9L8uvqf4Re7KYWV</recordid><startdate>20150901</startdate><enddate>20150901</enddate><creator>Ramachandran, V</creator><creator>Saravanan, R</creator><general>SAGE Publications</general><general>Sage Publications Ltd</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>3V.</scope><scope>7RV</scope><scope>7ST</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>SOI</scope></search><sort><creationdate>20150901</creationdate><title>Glucose uptake through translocation and activation of GLUT4 in PI3K/Akt signaling pathway by asiatic acid in diabetic rats</title><author>Ramachandran, V ; Saravanan, R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c473t-f71879f2545e30dc49676f9e2548da992a73713523e06f3aa4a2de29234615923</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Acids</topic><topic>Animals</topic><topic>Antioxidants - metabolism</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Experimental - blood</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Glucose</topic><topic>Glucose - metabolism</topic><topic>Glucose Transporter Type 4 - drug effects</topic><topic>Glucose Transporter Type 4 - metabolism</topic><topic>Insulin</topic><topic>Insulin - blood</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Male</topic><topic>Oncogene Protein v-akt - drug effects</topic><topic>Oncogene Protein v-akt - metabolism</topic><topic>Pentacyclic Triterpenes - pharmacology</topic><topic>Phosphatidylinositol 3-Kinases - drug effects</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptor, Insulin - biosynthesis</topic><topic>Rodents</topic><topic>Signal Transduction - drug effects</topic><topic>Studies</topic><topic>Thiobarbituric Acid Reactive Substances - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ramachandran, V</creatorcontrib><creatorcontrib>Saravanan, R</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Environment Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Environment Abstracts</collection><jtitle>Human & experimental toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Ramachandran, V</au><au>Saravanan, R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glucose uptake through translocation and activation of GLUT4 in PI3K/Akt signaling pathway by asiatic acid in diabetic rats</atitle><jtitle>Human & experimental toxicology</jtitle><addtitle>Hum Exp Toxicol</addtitle><date>2015-09-01</date><risdate>2015</risdate><volume>34</volume><issue>9</issue><spage>884</spage><epage>893</epage><pages>884-893</pages><issn>0960-3271</issn><eissn>1477-0903</eissn><abstract>In this study, we examined the in vivo effect and the mechanism of asiatic acid (AA) on glucose uptake in an insulin target skeletal muscle. Diabetic rats showed significantly increased levels of plasma glucose, thiobarbituric acid reactive substances, and lipid hydroperoxides, decreased levels of insulin and antioxidants, and impairment in insulin-signaling proteins such as insulin receptor (IR), insulin receptor substrate (IRS)-1/2, phosphoinositide 3-kinase (PI3K), Akt, and glucose transporter 4 (GLUT4) proteins. Oral treatment with AA (20 mg/kg body weight) showed near-normalized levels of plasma glucose, lipid peroxidation products, and antioxidants and improved insulin, IR, IRS-1/2, PI3K, Akt, and GLUT4 proteins. These findings suggest that AA improves glucose response by increasing GLUT4 in skeletal muscle through Akt and antioxidant defense in plasma and it also improves glucose homeostasis.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>26286522</pmid><doi>10.1177/0960327114561663</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acids Animals Antioxidants - metabolism Diabetes Diabetes Mellitus, Experimental - blood Diabetes Mellitus, Experimental - metabolism Glucose Glucose - metabolism Glucose Transporter Type 4 - drug effects Glucose Transporter Type 4 - metabolism Insulin Insulin - blood Lipid Peroxidation - drug effects Male Oncogene Protein v-akt - drug effects Oncogene Protein v-akt - metabolism Pentacyclic Triterpenes - pharmacology Phosphatidylinositol 3-Kinases - drug effects Phosphatidylinositol 3-Kinases - metabolism Rats Rats, Wistar Receptor, Insulin - biosynthesis Rodents Signal Transduction - drug effects Studies Thiobarbituric Acid Reactive Substances - metabolism |
| title | Glucose uptake through translocation and activation of GLUT4 in PI3K/Akt signaling pathway by asiatic acid in diabetic rats |
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