The Hepatic Protection Effects of Hepassocin in Hyperglycemic Crisis
Abstract Context: High glucose generates reactive oxygen species (ROS) and contributes to glucotoxicity in hepatocytes, and hyperglycemia causes structural and functional damage to the liver. However, only a mild hepatic dysfunction was observed in subjects with hyperglycemic crisis, implying a fact...
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| Veröffentlicht in: | The journal of clinical endocrinology and metabolism 2017-07, Vol.102 (7), p.2407-2415 |
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| creator | Ou, Horng-Yih Wu, Hung-Tsung Lin, Ching-Han Du, Ye-Fong Hu, Che-Yuan Hung, Hao-Chang Wu, Pansee Li, Hung-Yuan Wang, Shu-Huei Chang, Chih-Jen |
| description | Abstract
Context:
High glucose generates reactive oxygen species (ROS) and contributes to glucotoxicity in hepatocytes, and hyperglycemia causes structural and functional damage to the liver. However, only a mild hepatic dysfunction was observed in subjects with hyperglycemic crisis, implying a factor exists to exert a hepatic protective effect. Hepassocin is a hepatokine that modulates the proliferation and metabolism of hepatocytes and also exerts protective activity in liver injury. However, its role in hyperglycemic crisis-induced hepatic dysfunction remains unknown.
Objective:
To investigate the possible hepatic protection effects of hepassocin in hyperglycemic crisis.
Design, Setting, and Patients:
Plasma hepassocin concentrations and routine biochemistry were measured in 21 patients with hyperglycemic crisis before and after standard treatments. The effects of hepassocin on hepatic functions were evaluated in streptozotocin-induced hyperglycemic mice (STZ mice). HepG2 cells were used to clarify the possible mechanisms regulating hepassocin expression.
Results:
Plasma hepassocin concentrations decreased significantly in subjects with hyperglycemic crisis after standard treatment accompanied by improved hepatic functions. Correction of hyperglycemia in STZ mice also decreased the hepatic hepassocin expression. Injection of recombinant hepassocin improved hepatic functions and histologic changes and increased the expression of antioxidative stress proteins, including superoxide dismutase 1 (SOD1). In HepG2 cells, high glucose increased hepassocin expression through signal transducer and activator of transcription 3 and hepatocyte nuclear factor–related pathways. We also demonstrated that hepassocin increased SOD1 expression through an extracellular signal-regulated kinase 1/2 nuclear factor erythroid-2-related factor 2 pathway, decreasing ethyl acetate–induced ROS production and improving cell viability.
Conclusions:
Increased hepassocin secretion in hyperglycemic crisis might offset the deleterious effects of hyperglycemia on hepatocytes.
Elevated hepassocin secretion in hyperglycemic crisis offsets the deleterious effects of hyperglycemia on hepatocytes by increasing antioxidative proteins. |
| doi_str_mv | 10.1210/jc.2016-3287 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1887050839</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><oup_id>10.1210/jc.2016-3287</oup_id><sourcerecordid>1970003529</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4307-a682f1a8cc13680b7e287ba154f47f464e0aa36bbb0fbd884b9851beca7634043</originalsourceid><addsrcrecordid>eNp1kM9LHDEUx4NUdLXePJeBHtpDx778mEnmKFvtCoIeLHgLSXzpzjq7GZMZZP_7ZjtrD0Ih8ALv877v8SHknMIFZRS-r9wFA1qXnCl5QGa0EVUpaSM_kBkAo2Uj2eMxOUlpBUCFqPgROWZKAKsEzMiPhyUWC-zN0LriPoYB3dCGTXHlff6lIvi_3ZSCazdFfottj_F3t3W4zhPz2KY2fSSH3nQJz_b1lPy6vnqYL8rbu58388vb0gkOsjS1Yp4a5RzltQIrMZ9sDa2EF9KLWiAYw2trLXj7pJSwjaqoRWdkzQUIfkq-Trl9DC8jpkGv2-Sw68wGw5g0VUpCBYo3Gf38Dl2FMW7ydTq7AQBesR31baJcDClF9LqP7drEraagd3b1yumdXb2zm_FP-9DRrvHpH_ymMwMwAa-hGzCm5258xaiXaLph-T6z3Gd-mUbC2P9v-0T-ASn2jtk</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1970003529</pqid></control><display><type>article</type><title>The Hepatic Protection Effects of Hepassocin in Hyperglycemic Crisis</title><source>Oxford University Press Journals All Titles (1996-Current)</source><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><source>Journals@Ovid Complete</source><source>ProQuest Central</source><creator>Ou, Horng-Yih ; Wu, Hung-Tsung ; Lin, Ching-Han ; Du, Ye-Fong ; Hu, Che-Yuan ; Hung, Hao-Chang ; Wu, Pansee ; Li, Hung-Yuan ; Wang, Shu-Huei ; Chang, Chih-Jen</creator><creatorcontrib>Ou, Horng-Yih ; Wu, Hung-Tsung ; Lin, Ching-Han ; Du, Ye-Fong ; Hu, Che-Yuan ; Hung, Hao-Chang ; Wu, Pansee ; Li, Hung-Yuan ; Wang, Shu-Huei ; Chang, Chih-Jen</creatorcontrib><description>Abstract
Context:
High glucose generates reactive oxygen species (ROS) and contributes to glucotoxicity in hepatocytes, and hyperglycemia causes structural and functional damage to the liver. However, only a mild hepatic dysfunction was observed in subjects with hyperglycemic crisis, implying a factor exists to exert a hepatic protective effect. Hepassocin is a hepatokine that modulates the proliferation and metabolism of hepatocytes and also exerts protective activity in liver injury. However, its role in hyperglycemic crisis-induced hepatic dysfunction remains unknown.
Objective:
To investigate the possible hepatic protection effects of hepassocin in hyperglycemic crisis.
Design, Setting, and Patients:
Plasma hepassocin concentrations and routine biochemistry were measured in 21 patients with hyperglycemic crisis before and after standard treatments. The effects of hepassocin on hepatic functions were evaluated in streptozotocin-induced hyperglycemic mice (STZ mice). HepG2 cells were used to clarify the possible mechanisms regulating hepassocin expression.
Results:
Plasma hepassocin concentrations decreased significantly in subjects with hyperglycemic crisis after standard treatment accompanied by improved hepatic functions. Correction of hyperglycemia in STZ mice also decreased the hepatic hepassocin expression. Injection of recombinant hepassocin improved hepatic functions and histologic changes and increased the expression of antioxidative stress proteins, including superoxide dismutase 1 (SOD1). In HepG2 cells, high glucose increased hepassocin expression through signal transducer and activator of transcription 3 and hepatocyte nuclear factor–related pathways. We also demonstrated that hepassocin increased SOD1 expression through an extracellular signal-regulated kinase 1/2 nuclear factor erythroid-2-related factor 2 pathway, decreasing ethyl acetate–induced ROS production and improving cell viability.
Conclusions:
Increased hepassocin secretion in hyperglycemic crisis might offset the deleterious effects of hyperglycemia on hepatocytes.
Elevated hepassocin secretion in hyperglycemic crisis offsets the deleterious effects of hyperglycemia on hepatocytes by increasing antioxidative proteins.</description><identifier>ISSN: 0021-972X</identifier><identifier>EISSN: 1945-7197</identifier><identifier>DOI: 10.1210/jc.2016-3287</identifier><identifier>PMID: 28402540</identifier><language>eng</language><publisher>Washington, DC: Endocrine Society</publisher><subject>Acetic acid ; Adult ; Analysis of Variance ; Animals ; Blotting, Western ; Cells, Cultured ; Crises ; Disease Models, Animal ; Ethyl acetate ; Extracellular signal-regulated kinase ; Glucose ; Heat shock proteins ; Hep G2 Cells - metabolism ; Hepatocytes ; Humans ; Hyperglycemia ; Hyperglycemia - diagnosis ; Hyperglycemia - drug therapy ; Hypoglycemic Agents - administration & dosage ; Liver ; Liver Failure - prevention & control ; Male ; Metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Middle Aged ; Neoplasm Proteins - metabolism ; Proteins ; Random Allocation ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Real-Time Polymerase Chain Reaction - methods ; RNA, Small Interfering - metabolism ; Rodents ; Sampling Studies ; Secretion ; Streptozocin ; Streptozocin - pharmacology ; Stress proteins ; Structure-function relationships ; Superoxide dismutase ; Transcription ; Transfection</subject><ispartof>The journal of clinical endocrinology and metabolism, 2017-07, Vol.102 (7), p.2407-2415</ispartof><rights>Copyright © 2017 Endocrine Society 2017</rights><rights>Copyright © Oxford University Press 2015</rights><rights>Copyright © 2017 Endocrine Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4307-a682f1a8cc13680b7e287ba154f47f464e0aa36bbb0fbd884b9851beca7634043</citedby><cites>FETCH-LOGICAL-c4307-a682f1a8cc13680b7e287ba154f47f464e0aa36bbb0fbd884b9851beca7634043</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1970003529?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,776,780,21367,27901,27902,33721,33722,43781</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28402540$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ou, Horng-Yih</creatorcontrib><creatorcontrib>Wu, Hung-Tsung</creatorcontrib><creatorcontrib>Lin, Ching-Han</creatorcontrib><creatorcontrib>Du, Ye-Fong</creatorcontrib><creatorcontrib>Hu, Che-Yuan</creatorcontrib><creatorcontrib>Hung, Hao-Chang</creatorcontrib><creatorcontrib>Wu, Pansee</creatorcontrib><creatorcontrib>Li, Hung-Yuan</creatorcontrib><creatorcontrib>Wang, Shu-Huei</creatorcontrib><creatorcontrib>Chang, Chih-Jen</creatorcontrib><title>The Hepatic Protection Effects of Hepassocin in Hyperglycemic Crisis</title><title>The journal of clinical endocrinology and metabolism</title><addtitle>J Clin Endocrinol Metab</addtitle><description>Abstract
Context:
High glucose generates reactive oxygen species (ROS) and contributes to glucotoxicity in hepatocytes, and hyperglycemia causes structural and functional damage to the liver. However, only a mild hepatic dysfunction was observed in subjects with hyperglycemic crisis, implying a factor exists to exert a hepatic protective effect. Hepassocin is a hepatokine that modulates the proliferation and metabolism of hepatocytes and also exerts protective activity in liver injury. However, its role in hyperglycemic crisis-induced hepatic dysfunction remains unknown.
Objective:
To investigate the possible hepatic protection effects of hepassocin in hyperglycemic crisis.
Design, Setting, and Patients:
Plasma hepassocin concentrations and routine biochemistry were measured in 21 patients with hyperglycemic crisis before and after standard treatments. The effects of hepassocin on hepatic functions were evaluated in streptozotocin-induced hyperglycemic mice (STZ mice). HepG2 cells were used to clarify the possible mechanisms regulating hepassocin expression.
Results:
Plasma hepassocin concentrations decreased significantly in subjects with hyperglycemic crisis after standard treatment accompanied by improved hepatic functions. Correction of hyperglycemia in STZ mice also decreased the hepatic hepassocin expression. Injection of recombinant hepassocin improved hepatic functions and histologic changes and increased the expression of antioxidative stress proteins, including superoxide dismutase 1 (SOD1). In HepG2 cells, high glucose increased hepassocin expression through signal transducer and activator of transcription 3 and hepatocyte nuclear factor–related pathways. We also demonstrated that hepassocin increased SOD1 expression through an extracellular signal-regulated kinase 1/2 nuclear factor erythroid-2-related factor 2 pathway, decreasing ethyl acetate–induced ROS production and improving cell viability.
Conclusions:
Increased hepassocin secretion in hyperglycemic crisis might offset the deleterious effects of hyperglycemia on hepatocytes.
Elevated hepassocin secretion in hyperglycemic crisis offsets the deleterious effects of hyperglycemia on hepatocytes by increasing antioxidative proteins.</description><subject>Acetic acid</subject><subject>Adult</subject><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Blotting, Western</subject><subject>Cells, Cultured</subject><subject>Crises</subject><subject>Disease Models, Animal</subject><subject>Ethyl acetate</subject><subject>Extracellular signal-regulated kinase</subject><subject>Glucose</subject><subject>Heat shock proteins</subject><subject>Hep G2 Cells - metabolism</subject><subject>Hepatocytes</subject><subject>Humans</subject><subject>Hyperglycemia</subject><subject>Hyperglycemia - diagnosis</subject><subject>Hyperglycemia - drug therapy</subject><subject>Hypoglycemic Agents - administration & dosage</subject><subject>Liver</subject><subject>Liver Failure - prevention & control</subject><subject>Male</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Obese</subject><subject>Middle Aged</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Proteins</subject><subject>Random Allocation</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Real-Time Polymerase Chain Reaction - methods</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Rodents</subject><subject>Sampling Studies</subject><subject>Secretion</subject><subject>Streptozocin</subject><subject>Streptozocin - pharmacology</subject><subject>Stress proteins</subject><subject>Structure-function relationships</subject><subject>Superoxide dismutase</subject><subject>Transcription</subject><subject>Transfection</subject><issn>0021-972X</issn><issn>1945-7197</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kM9LHDEUx4NUdLXePJeBHtpDx778mEnmKFvtCoIeLHgLSXzpzjq7GZMZZP_7ZjtrD0Ih8ALv877v8SHknMIFZRS-r9wFA1qXnCl5QGa0EVUpaSM_kBkAo2Uj2eMxOUlpBUCFqPgROWZKAKsEzMiPhyUWC-zN0LriPoYB3dCGTXHlff6lIvi_3ZSCazdFfottj_F3t3W4zhPz2KY2fSSH3nQJz_b1lPy6vnqYL8rbu58388vb0gkOsjS1Yp4a5RzltQIrMZ9sDa2EF9KLWiAYw2trLXj7pJSwjaqoRWdkzQUIfkq-Trl9DC8jpkGv2-Sw68wGw5g0VUpCBYo3Gf38Dl2FMW7ydTq7AQBesR31baJcDClF9LqP7drEraagd3b1yumdXb2zm_FP-9DRrvHpH_ymMwMwAa-hGzCm5258xaiXaLph-T6z3Gd-mUbC2P9v-0T-ASn2jtk</recordid><startdate>20170701</startdate><enddate>20170701</enddate><creator>Ou, Horng-Yih</creator><creator>Wu, Hung-Tsung</creator><creator>Lin, Ching-Han</creator><creator>Du, Ye-Fong</creator><creator>Hu, Che-Yuan</creator><creator>Hung, Hao-Chang</creator><creator>Wu, Pansee</creator><creator>Li, Hung-Yuan</creator><creator>Wang, Shu-Huei</creator><creator>Chang, Chih-Jen</creator><general>Endocrine Society</general><general>Copyright Oxford University Press</general><general>Oxford University Press</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>7QP</scope><scope>7T5</scope><scope>7TM</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>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20170701</creationdate><title>The Hepatic Protection Effects of Hepassocin in Hyperglycemic Crisis</title><author>Ou, Horng-Yih ; Wu, Hung-Tsung ; Lin, Ching-Han ; Du, Ye-Fong ; Hu, Che-Yuan ; Hung, Hao-Chang ; Wu, Pansee ; Li, Hung-Yuan ; Wang, Shu-Huei ; Chang, Chih-Jen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4307-a682f1a8cc13680b7e287ba154f47f464e0aa36bbb0fbd884b9851beca7634043</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Acetic acid</topic><topic>Adult</topic><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Blotting, Western</topic><topic>Cells, Cultured</topic><topic>Crises</topic><topic>Disease Models, Animal</topic><topic>Ethyl acetate</topic><topic>Extracellular signal-regulated kinase</topic><topic>Glucose</topic><topic>Heat shock proteins</topic><topic>Hep G2 Cells - metabolism</topic><topic>Hepatocytes</topic><topic>Humans</topic><topic>Hyperglycemia</topic><topic>Hyperglycemia - diagnosis</topic><topic>Hyperglycemia - drug therapy</topic><topic>Hypoglycemic Agents - administration & dosage</topic><topic>Liver</topic><topic>Liver Failure - prevention & control</topic><topic>Male</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Obese</topic><topic>Middle Aged</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Proteins</topic><topic>Random Allocation</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Real-Time Polymerase Chain Reaction - methods</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Rodents</topic><topic>Sampling Studies</topic><topic>Secretion</topic><topic>Streptozocin</topic><topic>Streptozocin - pharmacology</topic><topic>Stress proteins</topic><topic>Structure-function relationships</topic><topic>Superoxide dismutase</topic><topic>Transcription</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ou, Horng-Yih</creatorcontrib><creatorcontrib>Wu, Hung-Tsung</creatorcontrib><creatorcontrib>Lin, Ching-Han</creatorcontrib><creatorcontrib>Du, Ye-Fong</creatorcontrib><creatorcontrib>Hu, Che-Yuan</creatorcontrib><creatorcontrib>Hung, Hao-Chang</creatorcontrib><creatorcontrib>Wu, Pansee</creatorcontrib><creatorcontrib>Li, Hung-Yuan</creatorcontrib><creatorcontrib>Wang, Shu-Huei</creatorcontrib><creatorcontrib>Chang, Chih-Jen</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>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids 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>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>The journal of clinical endocrinology and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ou, Horng-Yih</au><au>Wu, Hung-Tsung</au><au>Lin, Ching-Han</au><au>Du, Ye-Fong</au><au>Hu, Che-Yuan</au><au>Hung, Hao-Chang</au><au>Wu, Pansee</au><au>Li, Hung-Yuan</au><au>Wang, Shu-Huei</au><au>Chang, Chih-Jen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Hepatic Protection Effects of Hepassocin in Hyperglycemic Crisis</atitle><jtitle>The journal of clinical endocrinology and metabolism</jtitle><addtitle>J Clin Endocrinol Metab</addtitle><date>2017-07-01</date><risdate>2017</risdate><volume>102</volume><issue>7</issue><spage>2407</spage><epage>2415</epage><pages>2407-2415</pages><issn>0021-972X</issn><eissn>1945-7197</eissn><abstract>Abstract
Context:
High glucose generates reactive oxygen species (ROS) and contributes to glucotoxicity in hepatocytes, and hyperglycemia causes structural and functional damage to the liver. However, only a mild hepatic dysfunction was observed in subjects with hyperglycemic crisis, implying a factor exists to exert a hepatic protective effect. Hepassocin is a hepatokine that modulates the proliferation and metabolism of hepatocytes and also exerts protective activity in liver injury. However, its role in hyperglycemic crisis-induced hepatic dysfunction remains unknown.
Objective:
To investigate the possible hepatic protection effects of hepassocin in hyperglycemic crisis.
Design, Setting, and Patients:
Plasma hepassocin concentrations and routine biochemistry were measured in 21 patients with hyperglycemic crisis before and after standard treatments. The effects of hepassocin on hepatic functions were evaluated in streptozotocin-induced hyperglycemic mice (STZ mice). HepG2 cells were used to clarify the possible mechanisms regulating hepassocin expression.
Results:
Plasma hepassocin concentrations decreased significantly in subjects with hyperglycemic crisis after standard treatment accompanied by improved hepatic functions. Correction of hyperglycemia in STZ mice also decreased the hepatic hepassocin expression. Injection of recombinant hepassocin improved hepatic functions and histologic changes and increased the expression of antioxidative stress proteins, including superoxide dismutase 1 (SOD1). In HepG2 cells, high glucose increased hepassocin expression through signal transducer and activator of transcription 3 and hepatocyte nuclear factor–related pathways. We also demonstrated that hepassocin increased SOD1 expression through an extracellular signal-regulated kinase 1/2 nuclear factor erythroid-2-related factor 2 pathway, decreasing ethyl acetate–induced ROS production and improving cell viability.
Conclusions:
Increased hepassocin secretion in hyperglycemic crisis might offset the deleterious effects of hyperglycemia on hepatocytes.
Elevated hepassocin secretion in hyperglycemic crisis offsets the deleterious effects of hyperglycemia on hepatocytes by increasing antioxidative proteins.</abstract><cop>Washington, DC</cop><pub>Endocrine Society</pub><pmid>28402540</pmid><doi>10.1210/jc.2016-3287</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0021-972X |
| ispartof | The journal of clinical endocrinology and metabolism, 2017-07, Vol.102 (7), p.2407-2415 |
| issn | 0021-972X 1945-7197 |
| language | eng |
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| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection; Journals@Ovid Complete; ProQuest Central |
| subjects | Acetic acid Adult Analysis of Variance Animals Blotting, Western Cells, Cultured Crises Disease Models, Animal Ethyl acetate Extracellular signal-regulated kinase Glucose Heat shock proteins Hep G2 Cells - metabolism Hepatocytes Humans Hyperglycemia Hyperglycemia - diagnosis Hyperglycemia - drug therapy Hypoglycemic Agents - administration & dosage Liver Liver Failure - prevention & control Male Metabolism Mice Mice, Inbred C57BL Mice, Obese Middle Aged Neoplasm Proteins - metabolism Proteins Random Allocation Reactive oxygen species Reactive Oxygen Species - metabolism Real-Time Polymerase Chain Reaction - methods RNA, Small Interfering - metabolism Rodents Sampling Studies Secretion Streptozocin Streptozocin - pharmacology Stress proteins Structure-function relationships Superoxide dismutase Transcription Transfection |
| title | The Hepatic Protection Effects of Hepassocin in Hyperglycemic Crisis |
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