Oleanolic acid improves hepatic insulin resistance via antioxidant, hypolipidemic and anti-inflammatory effects
•Oleanolic acid (OA) improves hepatic insulin resistance in db/db mice.•OA inhibits mitochondrial oxidative stress via activation of Nrf2–GCLc signal.•OA suppresses hepatic lipid accumulation and inflammation. Insulin resistance is the hallmark of type 2 diabetes mellitus (T2DM), which is closely re...
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Veröffentlicht in: | Molecular and cellular endocrinology 2013-08, Vol.376 (1-2), p.70-80 |
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creator | Wang, Xin Liu, Rui Zhang, Wei Zhang, Xiaodi Liao, Nai Wang, Zhao Li, Wenli Qin, Xujun Hai, Chunxu |
description | •Oleanolic acid (OA) improves hepatic insulin resistance in db/db mice.•OA inhibits mitochondrial oxidative stress via activation of Nrf2–GCLc signal.•OA suppresses hepatic lipid accumulation and inflammation.
Insulin resistance is the hallmark of type 2 diabetes mellitus (T2DM), which is closely related to disorder of lipid metabolism. The study was designed to evaluate the effects of oleanolic acid (OA) on hepatic insulin resistance and underlying mechanisms in Lepdb/db obese diabetic mice. db/db Mice were administered with OA (20mg/kg/day, i.p.) for two weeks. OA reduced body weight, liver weight, and fat weight, and protected liver morphology and function. OA decreased fasting blood glucose, improved glucose and insulin tolerance, enhanced insulin signaling and inhibited gluconeogenesis. In livers, mitochondrial biogenesis, ultrastructure and function were influenced, accompanied by increased cellular and mitochondrial ROS production. OA inhibited all these changes, in which process Nrf2–GCLc mediated stabilization of mitochondrial glutathione pool may be involved. Moreover, OA decreased serum triglyceride, total cholesterol, LDL, HDL, and free fatty acids, increased serum HDL, and reduced hepatic lipid accumulation. Furthermore, inflammatory condition in db/db mice was improved by OA, as evidenced by decreased level of IL-1 β, IL-6, and TNFα in circulation and in liver. The evidence suggests that OA improves hepatic insulin resistance through inhibition of mitochondrial ROS, hypolipidemic and anti-inflammatory effects. The effectiveness of OA leads to interesting therapeutic perspectives. |
doi_str_mv | 10.1016/j.mce.2013.06.014 |
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Insulin resistance is the hallmark of type 2 diabetes mellitus (T2DM), which is closely related to disorder of lipid metabolism. The study was designed to evaluate the effects of oleanolic acid (OA) on hepatic insulin resistance and underlying mechanisms in Lepdb/db obese diabetic mice. db/db Mice were administered with OA (20mg/kg/day, i.p.) for two weeks. OA reduced body weight, liver weight, and fat weight, and protected liver morphology and function. OA decreased fasting blood glucose, improved glucose and insulin tolerance, enhanced insulin signaling and inhibited gluconeogenesis. In livers, mitochondrial biogenesis, ultrastructure and function were influenced, accompanied by increased cellular and mitochondrial ROS production. OA inhibited all these changes, in which process Nrf2–GCLc mediated stabilization of mitochondrial glutathione pool may be involved. Moreover, OA decreased serum triglyceride, total cholesterol, LDL, HDL, and free fatty acids, increased serum HDL, and reduced hepatic lipid accumulation. Furthermore, inflammatory condition in db/db mice was improved by OA, as evidenced by decreased level of IL-1 β, IL-6, and TNFα in circulation and in liver. The evidence suggests that OA improves hepatic insulin resistance through inhibition of mitochondrial ROS, hypolipidemic and anti-inflammatory effects. The effectiveness of OA leads to interesting therapeutic perspectives.</description><identifier>ISSN: 0303-7207</identifier><identifier>EISSN: 1872-8057</identifier><identifier>DOI: 10.1016/j.mce.2013.06.014</identifier><identifier>PMID: 23791844</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Animals ; anti-inflammatory activity ; Anti-Inflammatory Agents, Non-Steroidal - pharmacology ; antioxidants ; Antioxidants - pharmacology ; biogenesis ; blood glucose ; Blood Glucose - metabolism ; blood serum ; body weight ; Body Weight - drug effects ; Cellular ; cholesterol ; Cytokines - antagonists & inhibitors ; Cytokines - biosynthesis ; Diabetes Mellitus, Experimental - drug therapy ; Diabetes Mellitus, Experimental - metabolism ; Diabetes Mellitus, Type 2 - drug therapy ; Diabetes Mellitus, Type 2 - metabolism ; Dyslipidemia ; fasting ; free fatty acids ; Gluconeogenesis ; Glucose ; glutathione ; Hepatic insulin resistance ; high density lipoprotein ; Hypolipidemic Agents - pharmacology ; Inflammation ; Injections, Intraperitoneal ; Insulin ; Insulin - metabolism ; Insulin Resistance ; interleukin-1beta ; interleukin-6 ; lipid metabolism ; Lipid Metabolism - drug effects ; Liver ; Liver - drug effects ; Liver - metabolism ; low density lipoprotein ; Male ; Mice ; Mice, Transgenic ; Mitochondrial Turnover - drug effects ; Noise levels ; noninsulin-dependent diabetes mellitus ; Oleanolic acid ; Oleanolic Acid - pharmacology ; Organ Size - drug effects ; Reactive oxygen species ; Reactive Oxygen Species - antagonists & inhibitors ; Serums ; triacylglycerols ; tumor necrosis factor-alpha ; ultrastructure ; Weight reduction</subject><ispartof>Molecular and cellular endocrinology, 2013-08, Vol.376 (1-2), p.70-80</ispartof><rights>2013 Elsevier Ireland Ltd</rights><rights>Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c476t-33d5ddada5a1bcdba10830f2fda1b33f5ab4b41f0619d61aef7e897e2b301f673</citedby><cites>FETCH-LOGICAL-c476t-33d5ddada5a1bcdba10830f2fda1b33f5ab4b41f0619d61aef7e897e2b301f673</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.mce.2013.06.014$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23791844$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Xin</creatorcontrib><creatorcontrib>Liu, Rui</creatorcontrib><creatorcontrib>Zhang, Wei</creatorcontrib><creatorcontrib>Zhang, Xiaodi</creatorcontrib><creatorcontrib>Liao, Nai</creatorcontrib><creatorcontrib>Wang, Zhao</creatorcontrib><creatorcontrib>Li, Wenli</creatorcontrib><creatorcontrib>Qin, Xujun</creatorcontrib><creatorcontrib>Hai, Chunxu</creatorcontrib><title>Oleanolic acid improves hepatic insulin resistance via antioxidant, hypolipidemic and anti-inflammatory effects</title><title>Molecular and cellular endocrinology</title><addtitle>Mol Cell Endocrinol</addtitle><description>•Oleanolic acid (OA) improves hepatic insulin resistance in db/db mice.•OA inhibits mitochondrial oxidative stress via activation of Nrf2–GCLc signal.•OA suppresses hepatic lipid accumulation and inflammation.
Insulin resistance is the hallmark of type 2 diabetes mellitus (T2DM), which is closely related to disorder of lipid metabolism. The study was designed to evaluate the effects of oleanolic acid (OA) on hepatic insulin resistance and underlying mechanisms in Lepdb/db obese diabetic mice. db/db Mice were administered with OA (20mg/kg/day, i.p.) for two weeks. OA reduced body weight, liver weight, and fat weight, and protected liver morphology and function. OA decreased fasting blood glucose, improved glucose and insulin tolerance, enhanced insulin signaling and inhibited gluconeogenesis. In livers, mitochondrial biogenesis, ultrastructure and function were influenced, accompanied by increased cellular and mitochondrial ROS production. OA inhibited all these changes, in which process Nrf2–GCLc mediated stabilization of mitochondrial glutathione pool may be involved. Moreover, OA decreased serum triglyceride, total cholesterol, LDL, HDL, and free fatty acids, increased serum HDL, and reduced hepatic lipid accumulation. Furthermore, inflammatory condition in db/db mice was improved by OA, as evidenced by decreased level of IL-1 β, IL-6, and TNFα in circulation and in liver. The evidence suggests that OA improves hepatic insulin resistance through inhibition of mitochondrial ROS, hypolipidemic and anti-inflammatory effects. The effectiveness of OA leads to interesting therapeutic perspectives.</description><subject>Animals</subject><subject>anti-inflammatory activity</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</subject><subject>antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>biogenesis</subject><subject>blood glucose</subject><subject>Blood Glucose - metabolism</subject><subject>blood serum</subject><subject>body weight</subject><subject>Body Weight - drug effects</subject><subject>Cellular</subject><subject>cholesterol</subject><subject>Cytokines - antagonists & inhibitors</subject><subject>Cytokines - biosynthesis</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes Mellitus, Type 2 - drug therapy</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Dyslipidemia</subject><subject>fasting</subject><subject>free fatty acids</subject><subject>Gluconeogenesis</subject><subject>Glucose</subject><subject>glutathione</subject><subject>Hepatic insulin resistance</subject><subject>high density lipoprotein</subject><subject>Hypolipidemic Agents - pharmacology</subject><subject>Inflammation</subject><subject>Injections, Intraperitoneal</subject><subject>Insulin</subject><subject>Insulin - metabolism</subject><subject>Insulin Resistance</subject><subject>interleukin-1beta</subject><subject>interleukin-6</subject><subject>lipid metabolism</subject><subject>Lipid Metabolism - drug effects</subject><subject>Liver</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>low density lipoprotein</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Mitochondrial Turnover - drug effects</subject><subject>Noise levels</subject><subject>noninsulin-dependent diabetes mellitus</subject><subject>Oleanolic acid</subject><subject>Oleanolic Acid - pharmacology</subject><subject>Organ Size - drug effects</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - antagonists & inhibitors</subject><subject>Serums</subject><subject>triacylglycerols</subject><subject>tumor necrosis factor-alpha</subject><subject>ultrastructure</subject><subject>Weight reduction</subject><issn>0303-7207</issn><issn>1872-8057</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1v1DAQhi0EotvCD-ACOfZAwkycxIk4oaqUSpV6gJ6tiT2mXuULO7ti_z1etnDsaTTjZ16NHyHeIRQI2HzaFqPhogSUBTQFYPVCbLBVZd5CrV6KDUiQuSpBnYnzGLcAoOqyfS3OSqk6bKtqI-b7gWmaB28yMt5mflzCvOeYPfJCa5r6Ke4GP2WBo48rTYazvaeMptXPv71N9WP2eFhSwuItj8ecyf59zv3kBhpHWudwyNg5Nmt8I145GiK_faoX4uHr9Y-rb_nd_c3t1Ze73FSqWXMpbW0tWaoJe2N7QmgluNLZ1EvpauqrvkIHDXa2QWKnuO0Ul70EdI2SF-LylJu-82vHcdWjj4aHgSaed1Fj3SjoUDZdQvGEmjDHGNjpJfiRwkEj6KNnvdXJsz561tDo5DntvH-K3_Uj2_8b_8Qm4MMJcDRr-hl81A_fU0INgC3Kuk3E5xPBScPec9DReE5-rQ_JlLazf-aAP-f8mgs</recordid><startdate>20130825</startdate><enddate>20130825</enddate><creator>Wang, Xin</creator><creator>Liu, Rui</creator><creator>Zhang, Wei</creator><creator>Zhang, Xiaodi</creator><creator>Liao, Nai</creator><creator>Wang, Zhao</creator><creator>Li, Wenli</creator><creator>Qin, Xujun</creator><creator>Hai, Chunxu</creator><general>Elsevier Ireland Ltd</general><scope>FBQ</scope><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>7U5</scope><scope>8FD</scope><scope>L7M</scope></search><sort><creationdate>20130825</creationdate><title>Oleanolic acid improves hepatic insulin resistance via antioxidant, hypolipidemic and anti-inflammatory effects</title><author>Wang, Xin ; Liu, Rui ; Zhang, Wei ; Zhang, Xiaodi ; Liao, Nai ; Wang, Zhao ; Li, Wenli ; Qin, Xujun ; Hai, Chunxu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c476t-33d5ddada5a1bcdba10830f2fda1b33f5ab4b41f0619d61aef7e897e2b301f673</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>anti-inflammatory activity</topic><topic>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</topic><topic>antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>biogenesis</topic><topic>blood glucose</topic><topic>Blood Glucose - metabolism</topic><topic>blood serum</topic><topic>body weight</topic><topic>Body Weight - drug effects</topic><topic>Cellular</topic><topic>cholesterol</topic><topic>Cytokines - antagonists & inhibitors</topic><topic>Cytokines - biosynthesis</topic><topic>Diabetes Mellitus, Experimental - drug therapy</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetes Mellitus, Type 2 - drug therapy</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Dyslipidemia</topic><topic>fasting</topic><topic>free fatty acids</topic><topic>Gluconeogenesis</topic><topic>Glucose</topic><topic>glutathione</topic><topic>Hepatic insulin resistance</topic><topic>high density lipoprotein</topic><topic>Hypolipidemic Agents - pharmacology</topic><topic>Inflammation</topic><topic>Injections, Intraperitoneal</topic><topic>Insulin</topic><topic>Insulin - metabolism</topic><topic>Insulin Resistance</topic><topic>interleukin-1beta</topic><topic>interleukin-6</topic><topic>lipid metabolism</topic><topic>Lipid Metabolism - drug effects</topic><topic>Liver</topic><topic>Liver - drug effects</topic><topic>Liver - metabolism</topic><topic>low density lipoprotein</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Mitochondrial Turnover - drug effects</topic><topic>Noise levels</topic><topic>noninsulin-dependent diabetes mellitus</topic><topic>Oleanolic acid</topic><topic>Oleanolic Acid - pharmacology</topic><topic>Organ Size - drug effects</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - antagonists & inhibitors</topic><topic>Serums</topic><topic>triacylglycerols</topic><topic>tumor necrosis factor-alpha</topic><topic>ultrastructure</topic><topic>Weight reduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Xin</creatorcontrib><creatorcontrib>Liu, Rui</creatorcontrib><creatorcontrib>Zhang, Wei</creatorcontrib><creatorcontrib>Zhang, Xiaodi</creatorcontrib><creatorcontrib>Liao, Nai</creatorcontrib><creatorcontrib>Wang, Zhao</creatorcontrib><creatorcontrib>Li, Wenli</creatorcontrib><creatorcontrib>Qin, Xujun</creatorcontrib><creatorcontrib>Hai, Chunxu</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>Technology Research Database</collection><collection>Advanced Technologies Database with Aerospace</collection><jtitle>Molecular and cellular endocrinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Xin</au><au>Liu, Rui</au><au>Zhang, Wei</au><au>Zhang, Xiaodi</au><au>Liao, Nai</au><au>Wang, Zhao</au><au>Li, Wenli</au><au>Qin, Xujun</au><au>Hai, Chunxu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oleanolic acid improves hepatic insulin resistance via antioxidant, hypolipidemic and anti-inflammatory effects</atitle><jtitle>Molecular and cellular endocrinology</jtitle><addtitle>Mol Cell Endocrinol</addtitle><date>2013-08-25</date><risdate>2013</risdate><volume>376</volume><issue>1-2</issue><spage>70</spage><epage>80</epage><pages>70-80</pages><issn>0303-7207</issn><eissn>1872-8057</eissn><abstract>•Oleanolic acid (OA) improves hepatic insulin resistance in db/db mice.•OA inhibits mitochondrial oxidative stress via activation of Nrf2–GCLc signal.•OA suppresses hepatic lipid accumulation and inflammation.
Insulin resistance is the hallmark of type 2 diabetes mellitus (T2DM), which is closely related to disorder of lipid metabolism. The study was designed to evaluate the effects of oleanolic acid (OA) on hepatic insulin resistance and underlying mechanisms in Lepdb/db obese diabetic mice. db/db Mice were administered with OA (20mg/kg/day, i.p.) for two weeks. OA reduced body weight, liver weight, and fat weight, and protected liver morphology and function. OA decreased fasting blood glucose, improved glucose and insulin tolerance, enhanced insulin signaling and inhibited gluconeogenesis. In livers, mitochondrial biogenesis, ultrastructure and function were influenced, accompanied by increased cellular and mitochondrial ROS production. OA inhibited all these changes, in which process Nrf2–GCLc mediated stabilization of mitochondrial glutathione pool may be involved. Moreover, OA decreased serum triglyceride, total cholesterol, LDL, HDL, and free fatty acids, increased serum HDL, and reduced hepatic lipid accumulation. Furthermore, inflammatory condition in db/db mice was improved by OA, as evidenced by decreased level of IL-1 β, IL-6, and TNFα in circulation and in liver. The evidence suggests that OA improves hepatic insulin resistance through inhibition of mitochondrial ROS, hypolipidemic and anti-inflammatory effects. The effectiveness of OA leads to interesting therapeutic perspectives.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>23791844</pmid><doi>10.1016/j.mce.2013.06.014</doi><tpages>11</tpages></addata></record> |
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subjects | Animals anti-inflammatory activity Anti-Inflammatory Agents, Non-Steroidal - pharmacology antioxidants Antioxidants - pharmacology biogenesis blood glucose Blood Glucose - metabolism blood serum body weight Body Weight - drug effects Cellular cholesterol Cytokines - antagonists & inhibitors Cytokines - biosynthesis Diabetes Mellitus, Experimental - drug therapy Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - metabolism Dyslipidemia fasting free fatty acids Gluconeogenesis Glucose glutathione Hepatic insulin resistance high density lipoprotein Hypolipidemic Agents - pharmacology Inflammation Injections, Intraperitoneal Insulin Insulin - metabolism Insulin Resistance interleukin-1beta interleukin-6 lipid metabolism Lipid Metabolism - drug effects Liver Liver - drug effects Liver - metabolism low density lipoprotein Male Mice Mice, Transgenic Mitochondrial Turnover - drug effects Noise levels noninsulin-dependent diabetes mellitus Oleanolic acid Oleanolic Acid - pharmacology Organ Size - drug effects Reactive oxygen species Reactive Oxygen Species - antagonists & inhibitors Serums triacylglycerols tumor necrosis factor-alpha ultrastructure Weight reduction |
title | Oleanolic acid improves hepatic insulin resistance via antioxidant, hypolipidemic and anti-inflammatory effects |
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