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Hepatosteatosis and hepatic insulin resistance are blunted by argirein, an anti-inflammatory agent, through normalizing endoplasmic reticulum stress and apoptosis in diabetic liver
Objectives Insulin resistance represents a mechanism underlying defect metabolism of carbohydrate and lipid linked to inflammatory reactions in diabetic liver. We hypothesized that the changes may be secondary to endoplasmic reticulum (ER) stress, which could be alleviated by either argirein or vals...
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| Published in: | Journal of pharmacy and pharmacology 2013-06, Vol.65 (6), p.916-927 |
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| container_end_page | 927 |
| container_issue | 6 |
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| container_title | Journal of pharmacy and pharmacology |
| container_volume | 65 |
| creator | Shi, Fang-Hong Wu, You Dai, De-Zai Cong, Xiao-Dong Zhang, Yu-Mao Dai, Yin |
| description | Objectives
Insulin resistance represents a mechanism underlying defect metabolism of carbohydrate and lipid linked to inflammatory reactions in diabetic liver. We hypothesized that the changes may be secondary to endoplasmic reticulum (ER) stress, which could be alleviated by either argirein or valsartan.
Methods
Hepatosteatosis in diabetic liver was induced in rats fed with a high‐fat diet (HFD) for 12 weeks combined with a single low dose of streptozotocin (STZ 35 mg/kg, ip). Interventions (mg/kg/d, po)with either argirein (50, 100 and 200) or valsartan (12) were conducted in the last 4 weeks.
Key findings
In diabetic liver fat was significantly accumulated in association with elevated hepatic glucose, serum insulin and homeostasis model assessment of insulin resistance value. Downregulated glucose transporter 4, insulin receptor substrate‐1 and leptin receptor (P |
| doi_str_mv | 10.1111/jphp.12051 |
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| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_1348552317</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2962228801</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4311-61c8273ee76af3b0804d041608938377c5bf87d16dfa79beba09f64b085ba52f3</originalsourceid><addsrcrecordid>eNp9kc1u1DAUhS0EokNhwwMgS-xQU_wT25klqqADqmCEipDYWHZyM-PBcVI7AYbn4gFxSNsllmXLvt8950oHoeeUnNO8Xh-G_XBOGRH0AVoxUrJCUVE9RCtCGCu4UPwEPUnpQAhRUsrH6IRxWSpZiRX6s4HBjH0aYT5dwiY0eD__uRq7kCbvAo6QK6MJNWATAVs_hREabI_5uXMRXDjLfXmPrnCh9abrslrM5R2E8QyP-9hPuz0OfeyMd79d2GEITT94k7rsEyG7TX7qcBqz1zKEGfphGSlP0DhjZwh79wPiU_SoNT7Bs9v7FH159_b6YlNcfbp8f_HmqqhLTmkhaV0xxQGUNC23pCJlQ0oqSbXmFVeqFratVENl0xq1tmANWbeyzKCwRrCWn6KXi-4Q-5sJ0qgP_RRDttSUl5UQjFOVqVcLVcc-pQitHqLrTDxqSvQckJ4D0v8CyvCLW8nJdtDco3eJZIAuwE_n4fgfKf1hu9neiRZLT04Jft33mPhdS8WV0F8_XurN5-ut3JbfdMn_AmHZr1o</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1348552317</pqid></control><display><type>article</type><title>Hepatosteatosis and hepatic insulin resistance are blunted by argirein, an anti-inflammatory agent, through normalizing endoplasmic reticulum stress and apoptosis in diabetic liver</title><source>Oxford Journals Online</source><creator>Shi, Fang-Hong ; Wu, You ; Dai, De-Zai ; Cong, Xiao-Dong ; Zhang, Yu-Mao ; Dai, Yin</creator><creatorcontrib>Shi, Fang-Hong ; Wu, You ; Dai, De-Zai ; Cong, Xiao-Dong ; Zhang, Yu-Mao ; Dai, Yin</creatorcontrib><description>Objectives
Insulin resistance represents a mechanism underlying defect metabolism of carbohydrate and lipid linked to inflammatory reactions in diabetic liver. We hypothesized that the changes may be secondary to endoplasmic reticulum (ER) stress, which could be alleviated by either argirein or valsartan.
Methods
Hepatosteatosis in diabetic liver was induced in rats fed with a high‐fat diet (HFD) for 12 weeks combined with a single low dose of streptozotocin (STZ 35 mg/kg, ip). Interventions (mg/kg/d, po)with either argirein (50, 100 and 200) or valsartan (12) were conducted in the last 4 weeks.
Key findings
In diabetic liver fat was significantly accumulated in association with elevated hepatic glucose, serum insulin and homeostasis model assessment of insulin resistance value. Downregulated glucose transporter 4, insulin receptor substrate‐1 and leptin receptor (P < 0.01) were found relative to normal, where DNA ladder, downregulated B cell lymphoma/leukemia‐2, upregulated B cell lymphoma/leukemia‐2 Associated X protein and upregulated ER stress chaperones such as Bip/GRP78 (also known as Binding Protein, BiP), PKR‐like ER kinase (PERK), p‐PERK/PERK and C/EBP homologous protein were significant. These abnormalities were significantly ameliorated by argirein and valsartan.
Conclusions
Hepatosteatosis induced by HFD/low STZ manifests insulin resistance and apoptosis, linked to an entity of low‐grade inflammation due to activated ER stress sensors. With anti‐inflammatory activity either argirein or valsartan blunts hepatosteatosis through normalizing ER stress and apoptosis in the diabetic liver.</description><identifier>ISSN: 0022-3573</identifier><identifier>EISSN: 2042-7158</identifier><identifier>DOI: 10.1111/jphp.12051</identifier><identifier>PMID: 23647685</identifier><identifier>CODEN: JPPMAB</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Animals ; Anthraquinones - pharmacology ; Anti-Inflammatory Agents - pharmacology ; apoptosis ; Apoptosis - drug effects ; Arginine - pharmacology ; argirein ; Cells ; Diabetes Mellitus, Experimental - blood ; Diabetes Mellitus, Experimental - drug therapy ; Diabetes Mellitus, Experimental - metabolism ; Diet, High-Fat - adverse effects ; Drug Combinations ; eIF-2 Kinase - metabolism ; Endoplasmic Reticulum Stress - drug effects ; ER stress ; Glucose - metabolism ; Glucose Transporter Type 4 - metabolism ; GluT4 ; Glutathione Peroxidase - blood ; Glutathione Peroxidase - metabolism ; Glycogen - metabolism ; Heat-Shock Proteins - metabolism ; hepatosteatosis ; Insulin - blood ; Insulin - metabolism ; Insulin Receptor Substrate Proteins - metabolism ; Insulin resistance ; Insulin Resistance - physiology ; IRS-1 ; Liver - drug effects ; Liver - metabolism ; Lymphoma ; Male ; PPAR alpha - metabolism ; PPAR gamma - metabolism ; Proteins ; Rats ; Rats, Sprague-Dawley ; Receptors, Leptin - metabolism ; Rodents ; Tetrazoles - pharmacology ; Transcription Factor CHOP - metabolism ; Valine - analogs & derivatives ; Valine - pharmacology ; Valsartan</subject><ispartof>Journal of pharmacy and pharmacology, 2013-06, Vol.65 (6), p.916-927</ispartof><rights>2013 Royal Pharmaceutical Society</rights><rights>2013 Royal Pharmaceutical Society.</rights><rights>Copyright © 2013 Royal Pharmaceutical Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4311-61c8273ee76af3b0804d041608938377c5bf87d16dfa79beba09f64b085ba52f3</citedby><cites>FETCH-LOGICAL-c4311-61c8273ee76af3b0804d041608938377c5bf87d16dfa79beba09f64b085ba52f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23647685$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shi, Fang-Hong</creatorcontrib><creatorcontrib>Wu, You</creatorcontrib><creatorcontrib>Dai, De-Zai</creatorcontrib><creatorcontrib>Cong, Xiao-Dong</creatorcontrib><creatorcontrib>Zhang, Yu-Mao</creatorcontrib><creatorcontrib>Dai, Yin</creatorcontrib><title>Hepatosteatosis and hepatic insulin resistance are blunted by argirein, an anti-inflammatory agent, through normalizing endoplasmic reticulum stress and apoptosis in diabetic liver</title><title>Journal of pharmacy and pharmacology</title><addtitle>J Pharm Pharmacol</addtitle><description>Objectives
Insulin resistance represents a mechanism underlying defect metabolism of carbohydrate and lipid linked to inflammatory reactions in diabetic liver. We hypothesized that the changes may be secondary to endoplasmic reticulum (ER) stress, which could be alleviated by either argirein or valsartan.
Methods
Hepatosteatosis in diabetic liver was induced in rats fed with a high‐fat diet (HFD) for 12 weeks combined with a single low dose of streptozotocin (STZ 35 mg/kg, ip). Interventions (mg/kg/d, po)with either argirein (50, 100 and 200) or valsartan (12) were conducted in the last 4 weeks.
Key findings
In diabetic liver fat was significantly accumulated in association with elevated hepatic glucose, serum insulin and homeostasis model assessment of insulin resistance value. Downregulated glucose transporter 4, insulin receptor substrate‐1 and leptin receptor (P < 0.01) were found relative to normal, where DNA ladder, downregulated B cell lymphoma/leukemia‐2, upregulated B cell lymphoma/leukemia‐2 Associated X protein and upregulated ER stress chaperones such as Bip/GRP78 (also known as Binding Protein, BiP), PKR‐like ER kinase (PERK), p‐PERK/PERK and C/EBP homologous protein were significant. These abnormalities were significantly ameliorated by argirein and valsartan.
Conclusions
Hepatosteatosis induced by HFD/low STZ manifests insulin resistance and apoptosis, linked to an entity of low‐grade inflammation due to activated ER stress sensors. With anti‐inflammatory activity either argirein or valsartan blunts hepatosteatosis through normalizing ER stress and apoptosis in the diabetic liver.</description><subject>Animals</subject><subject>Anthraquinones - pharmacology</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Arginine - pharmacology</subject><subject>argirein</subject><subject>Cells</subject><subject>Diabetes Mellitus, Experimental - blood</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diet, High-Fat - adverse effects</subject><subject>Drug Combinations</subject><subject>eIF-2 Kinase - metabolism</subject><subject>Endoplasmic Reticulum Stress - drug effects</subject><subject>ER stress</subject><subject>Glucose - metabolism</subject><subject>Glucose Transporter Type 4 - metabolism</subject><subject>GluT4</subject><subject>Glutathione Peroxidase - blood</subject><subject>Glutathione Peroxidase - metabolism</subject><subject>Glycogen - metabolism</subject><subject>Heat-Shock Proteins - metabolism</subject><subject>hepatosteatosis</subject><subject>Insulin - blood</subject><subject>Insulin - metabolism</subject><subject>Insulin Receptor Substrate Proteins - metabolism</subject><subject>Insulin resistance</subject><subject>Insulin Resistance - physiology</subject><subject>IRS-1</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>Lymphoma</subject><subject>Male</subject><subject>PPAR alpha - metabolism</subject><subject>PPAR gamma - metabolism</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Leptin - metabolism</subject><subject>Rodents</subject><subject>Tetrazoles - pharmacology</subject><subject>Transcription Factor CHOP - metabolism</subject><subject>Valine - analogs & derivatives</subject><subject>Valine - pharmacology</subject><subject>Valsartan</subject><issn>0022-3573</issn><issn>2042-7158</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNp9kc1u1DAUhS0EokNhwwMgS-xQU_wT25klqqADqmCEipDYWHZyM-PBcVI7AYbn4gFxSNsllmXLvt8950oHoeeUnNO8Xh-G_XBOGRH0AVoxUrJCUVE9RCtCGCu4UPwEPUnpQAhRUsrH6IRxWSpZiRX6s4HBjH0aYT5dwiY0eD__uRq7kCbvAo6QK6MJNWATAVs_hREabI_5uXMRXDjLfXmPrnCh9abrslrM5R2E8QyP-9hPuz0OfeyMd79d2GEITT94k7rsEyG7TX7qcBqz1zKEGfphGSlP0DhjZwh79wPiU_SoNT7Bs9v7FH159_b6YlNcfbp8f_HmqqhLTmkhaV0xxQGUNC23pCJlQ0oqSbXmFVeqFratVENl0xq1tmANWbeyzKCwRrCWn6KXi-4Q-5sJ0qgP_RRDttSUl5UQjFOVqVcLVcc-pQitHqLrTDxqSvQckJ4D0v8CyvCLW8nJdtDco3eJZIAuwE_n4fgfKf1hu9neiRZLT04Jft33mPhdS8WV0F8_XurN5-ut3JbfdMn_AmHZr1o</recordid><startdate>201306</startdate><enddate>201306</enddate><creator>Shi, Fang-Hong</creator><creator>Wu, You</creator><creator>Dai, De-Zai</creator><creator>Cong, Xiao-Dong</creator><creator>Zhang, Yu-Mao</creator><creator>Dai, Yin</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</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>7QP</scope><scope>7TK</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope></search><sort><creationdate>201306</creationdate><title>Hepatosteatosis and hepatic insulin resistance are blunted by argirein, an anti-inflammatory agent, through normalizing endoplasmic reticulum stress and apoptosis in diabetic liver</title><author>Shi, Fang-Hong ; Wu, You ; Dai, De-Zai ; Cong, Xiao-Dong ; Zhang, Yu-Mao ; Dai, Yin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4311-61c8273ee76af3b0804d041608938377c5bf87d16dfa79beba09f64b085ba52f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Anthraquinones - pharmacology</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Arginine - pharmacology</topic><topic>argirein</topic><topic>Cells</topic><topic>Diabetes Mellitus, Experimental - blood</topic><topic>Diabetes Mellitus, Experimental - drug therapy</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diet, High-Fat - adverse effects</topic><topic>Drug Combinations</topic><topic>eIF-2 Kinase - metabolism</topic><topic>Endoplasmic Reticulum Stress - drug effects</topic><topic>ER stress</topic><topic>Glucose - metabolism</topic><topic>Glucose Transporter Type 4 - metabolism</topic><topic>GluT4</topic><topic>Glutathione Peroxidase - blood</topic><topic>Glutathione Peroxidase - metabolism</topic><topic>Glycogen - metabolism</topic><topic>Heat-Shock Proteins - metabolism</topic><topic>hepatosteatosis</topic><topic>Insulin - blood</topic><topic>Insulin - metabolism</topic><topic>Insulin Receptor Substrate Proteins - metabolism</topic><topic>Insulin resistance</topic><topic>Insulin Resistance - physiology</topic><topic>IRS-1</topic><topic>Liver - drug effects</topic><topic>Liver - metabolism</topic><topic>Lymphoma</topic><topic>Male</topic><topic>PPAR alpha - metabolism</topic><topic>PPAR gamma - metabolism</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Leptin - metabolism</topic><topic>Rodents</topic><topic>Tetrazoles - pharmacology</topic><topic>Transcription Factor CHOP - metabolism</topic><topic>Valine - analogs & derivatives</topic><topic>Valine - pharmacology</topic><topic>Valsartan</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shi, Fang-Hong</creatorcontrib><creatorcontrib>Wu, You</creatorcontrib><creatorcontrib>Dai, De-Zai</creatorcontrib><creatorcontrib>Cong, Xiao-Dong</creatorcontrib><creatorcontrib>Zhang, Yu-Mao</creatorcontrib><creatorcontrib>Dai, Yin</creatorcontrib><collection>Istex</collection><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>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><jtitle>Journal of pharmacy and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shi, Fang-Hong</au><au>Wu, You</au><au>Dai, De-Zai</au><au>Cong, Xiao-Dong</au><au>Zhang, Yu-Mao</au><au>Dai, Yin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hepatosteatosis and hepatic insulin resistance are blunted by argirein, an anti-inflammatory agent, through normalizing endoplasmic reticulum stress and apoptosis in diabetic liver</atitle><jtitle>Journal of pharmacy and pharmacology</jtitle><addtitle>J Pharm Pharmacol</addtitle><date>2013-06</date><risdate>2013</risdate><volume>65</volume><issue>6</issue><spage>916</spage><epage>927</epage><pages>916-927</pages><issn>0022-3573</issn><eissn>2042-7158</eissn><coden>JPPMAB</coden><abstract>Objectives
Insulin resistance represents a mechanism underlying defect metabolism of carbohydrate and lipid linked to inflammatory reactions in diabetic liver. We hypothesized that the changes may be secondary to endoplasmic reticulum (ER) stress, which could be alleviated by either argirein or valsartan.
Methods
Hepatosteatosis in diabetic liver was induced in rats fed with a high‐fat diet (HFD) for 12 weeks combined with a single low dose of streptozotocin (STZ 35 mg/kg, ip). Interventions (mg/kg/d, po)with either argirein (50, 100 and 200) or valsartan (12) were conducted in the last 4 weeks.
Key findings
In diabetic liver fat was significantly accumulated in association with elevated hepatic glucose, serum insulin and homeostasis model assessment of insulin resistance value. Downregulated glucose transporter 4, insulin receptor substrate‐1 and leptin receptor (P < 0.01) were found relative to normal, where DNA ladder, downregulated B cell lymphoma/leukemia‐2, upregulated B cell lymphoma/leukemia‐2 Associated X protein and upregulated ER stress chaperones such as Bip/GRP78 (also known as Binding Protein, BiP), PKR‐like ER kinase (PERK), p‐PERK/PERK and C/EBP homologous protein were significant. These abnormalities were significantly ameliorated by argirein and valsartan.
Conclusions
Hepatosteatosis induced by HFD/low STZ manifests insulin resistance and apoptosis, linked to an entity of low‐grade inflammation due to activated ER stress sensors. With anti‐inflammatory activity either argirein or valsartan blunts hepatosteatosis through normalizing ER stress and apoptosis in the diabetic liver.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>23647685</pmid><doi>10.1111/jphp.12051</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of pharmacy and pharmacology, 2013-06, Vol.65 (6), p.916-927 |
| issn | 0022-3573 2042-7158 |
| language | eng |
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| source | Oxford Journals Online |
| subjects | Animals Anthraquinones - pharmacology Anti-Inflammatory Agents - pharmacology apoptosis Apoptosis - drug effects Arginine - pharmacology argirein Cells Diabetes Mellitus, Experimental - blood Diabetes Mellitus, Experimental - drug therapy Diabetes Mellitus, Experimental - metabolism Diet, High-Fat - adverse effects Drug Combinations eIF-2 Kinase - metabolism Endoplasmic Reticulum Stress - drug effects ER stress Glucose - metabolism Glucose Transporter Type 4 - metabolism GluT4 Glutathione Peroxidase - blood Glutathione Peroxidase - metabolism Glycogen - metabolism Heat-Shock Proteins - metabolism hepatosteatosis Insulin - blood Insulin - metabolism Insulin Receptor Substrate Proteins - metabolism Insulin resistance Insulin Resistance - physiology IRS-1 Liver - drug effects Liver - metabolism Lymphoma Male PPAR alpha - metabolism PPAR gamma - metabolism Proteins Rats Rats, Sprague-Dawley Receptors, Leptin - metabolism Rodents Tetrazoles - pharmacology Transcription Factor CHOP - metabolism Valine - analogs & derivatives Valine - pharmacology Valsartan |
| title | Hepatosteatosis and hepatic insulin resistance are blunted by argirein, an anti-inflammatory agent, through normalizing endoplasmic reticulum stress and apoptosis in diabetic liver |
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