Regulation of glucose lipid metabolism and insulin sensitivity by interleukin-4
Objective: Abundant evidence has demonstrated that long-term cytokine-mediated inflammation is a risk factor for obesity and type 2 diabetes mellitus (T2DM). Our previous study reveals a significant association between promoter polymorphisms of Th2-derived cytokine interleukin-4 (IL-4) and T2DM, whi...
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| Veröffentlicht in: | International Journal of Obesity 2012-07, Vol.36 (7), p.993-998 |
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| container_title | International Journal of Obesity |
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| creator | Chang, Y-H Ho, K-T Lu, S-H Huang, C-N Shiau, M-Y |
| description | Objective:
Abundant evidence has demonstrated that long-term cytokine-mediated inflammation is a risk factor for obesity and type 2 diabetes mellitus (T2DM). Our previous study reveals a significant association between promoter polymorphisms of Th2-derived cytokine interleukin-4 (IL-4) and T2DM, which suggests possible roles of IL-4 in metabolism. In this study, we focused on examining the putative regulation of glucose and lipid metabolism by IL-4.
Methods:
C57BL/6 mice were intraperitoneally injected with either adenovirus containing full-length IL-4 encoding gene (AdIL-4) or recombinant IL-4 for mimicking the status of transient and long-term IL-4 overexpression, respectively, and the effects of the overexpressed IL-4 to glucose/lipid metabolism and insulin sensitivity were subsequently investigated.
Results:
Our results reveal that IL-4 improves insulin sensitivity and glucose tolerance through upregulating Akt phosphorylation while attenuating GSK-3β activities. IL-4 is also involved in lipid metabolism by inhibiting lipid accumulation in fat tissues, which lead to decreased weight gain and fat mass.
Conclusions:
Our results suggest that IL-4 regulates glucose and lipid metabolism by promoting insulin sensitivity, glucose tolerance and inhibiting lipid deposits. This study uncovers the novel roles of IL-4 in metabolism and provides new insights in the interaction between cytokines/immune responses, insulin sensitivity and metabolism. |
| doi_str_mv | 10.1038/ijo.2011.168 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_1024478894</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A297040316</galeid><sourcerecordid>A297040316</sourcerecordid><originalsourceid>FETCH-LOGICAL-c510t-1a9ad8a7376b15d5666c91de2c30fa121f500655ac7e1f17485439616e338b3b3</originalsourceid><addsrcrecordid>eNpt0dtrFDEUB-Agil2rbz7LgCg-OGsyuczMYyneoFAQfQ6ZzJlt1kyy5lLY_96Mu9atlPMQSL6cXH4IvSR4TTDtPpitXzeYkDUR3SO0IqwVNWd9-xitMMVtjbngZ-hZjFuMMee4eYrOGtL1jAi8QtffYJOtSsa7yk_VxmbtI1TW7MxYzZDU4K2Jc6XcWBkXszWuiuCiSebWpH017Mt0gmAh_zSuZs_Rk0nZCC-O4zn68enj98sv9dX156-XF1e15gSnmqhejZ1qaSsGwkcuhNA9GaHRFE-KNGTiGAvOlW6BTKRlHWe0F0QApd1AB3qO3h367oL_lSEmOZuowVrlwOcoCW4Ya7vyzEJf_0e3PgdXbvdHleqaE7VRFqRxk09B6aWpvGj6FjNMiShq_YAqNcJstHcwmTJ_b8Pbkw03oGy6id7m5cPjffj-AHXwMQaY5C6YWYV9uaRcgpYlaLkELUvQhb86PioPM4x3-G-yBbw5AhW1slNQTpv4z4nSk-HF1QcXy5LbQDj9nQcPrg7eqZQD3DUsaDEL-Q1IWMY-</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1024242824</pqid></control><display><type>article</type><title>Regulation of glucose lipid metabolism and insulin sensitivity by interleukin-4</title><source>MEDLINE</source><source>Nature Journals Online</source><source>EZB-FREE-00999 freely available EZB journals</source><source>SpringerLink Journals - AutoHoldings</source><creator>Chang, Y-H ; Ho, K-T ; Lu, S-H ; Huang, C-N ; Shiau, M-Y</creator><creatorcontrib>Chang, Y-H ; Ho, K-T ; Lu, S-H ; Huang, C-N ; Shiau, M-Y</creatorcontrib><description>Objective:
Abundant evidence has demonstrated that long-term cytokine-mediated inflammation is a risk factor for obesity and type 2 diabetes mellitus (T2DM). Our previous study reveals a significant association between promoter polymorphisms of Th2-derived cytokine interleukin-4 (IL-4) and T2DM, which suggests possible roles of IL-4 in metabolism. In this study, we focused on examining the putative regulation of glucose and lipid metabolism by IL-4.
Methods:
C57BL/6 mice were intraperitoneally injected with either adenovirus containing full-length IL-4 encoding gene (AdIL-4) or recombinant IL-4 for mimicking the status of transient and long-term IL-4 overexpression, respectively, and the effects of the overexpressed IL-4 to glucose/lipid metabolism and insulin sensitivity were subsequently investigated.
Results:
Our results reveal that IL-4 improves insulin sensitivity and glucose tolerance through upregulating Akt phosphorylation while attenuating GSK-3β activities. IL-4 is also involved in lipid metabolism by inhibiting lipid accumulation in fat tissues, which lead to decreased weight gain and fat mass.
Conclusions:
Our results suggest that IL-4 regulates glucose and lipid metabolism by promoting insulin sensitivity, glucose tolerance and inhibiting lipid deposits. This study uncovers the novel roles of IL-4 in metabolism and provides new insights in the interaction between cytokines/immune responses, insulin sensitivity and metabolism.</description><identifier>ISSN: 0307-0565</identifier><identifier>EISSN: 1476-5497</identifier><identifier>DOI: 10.1038/ijo.2011.168</identifier><identifier>PMID: 21894160</identifier><identifier>CODEN: IJOBDP</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Adenoviruses ; Animals ; Biological and medical sciences ; Blood Glucose - metabolism ; Complications and side effects ; Cytokines ; Diabetes ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Epidemiology ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Gene Expression Regulation - genetics ; Genetic aspects ; Glucose ; Glucose metabolism ; Glucose Tolerance Test ; Glycogen Synthase Kinase 3 - metabolism ; Glycogen Synthase Kinase 3 beta ; Health Promotion and Disease Prevention ; Humans ; Insulin ; Insulin resistance ; Insulin Resistance - genetics ; Interleukin-4 ; Interleukin-4 - metabolism ; Internal Medicine ; Laboratory animals ; Lipid metabolism ; Lipid Metabolism - genetics ; Lipids ; Medical sciences ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Metabolism ; Mice ; Mice, Inbred C57BL ; Obesity ; Obesity - metabolism ; original-article ; Phosphorylation ; Physiological aspects ; Public Health ; Risk factors</subject><ispartof>International Journal of Obesity, 2012-07, Vol.36 (7), p.993-998</ispartof><rights>Macmillan Publishers Limited 2012</rights><rights>2015 INIST-CNRS</rights><rights>COPYRIGHT 2012 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jul 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c510t-1a9ad8a7376b15d5666c91de2c30fa121f500655ac7e1f17485439616e338b3b3</citedby><cites>FETCH-LOGICAL-c510t-1a9ad8a7376b15d5666c91de2c30fa121f500655ac7e1f17485439616e338b3b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/ijo.2011.168$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/ijo.2011.168$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,2727,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26103400$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21894160$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chang, Y-H</creatorcontrib><creatorcontrib>Ho, K-T</creatorcontrib><creatorcontrib>Lu, S-H</creatorcontrib><creatorcontrib>Huang, C-N</creatorcontrib><creatorcontrib>Shiau, M-Y</creatorcontrib><title>Regulation of glucose lipid metabolism and insulin sensitivity by interleukin-4</title><title>International Journal of Obesity</title><addtitle>Int J Obes</addtitle><addtitle>Int J Obes (Lond)</addtitle><description>Objective:
Abundant evidence has demonstrated that long-term cytokine-mediated inflammation is a risk factor for obesity and type 2 diabetes mellitus (T2DM). Our previous study reveals a significant association between promoter polymorphisms of Th2-derived cytokine interleukin-4 (IL-4) and T2DM, which suggests possible roles of IL-4 in metabolism. In this study, we focused on examining the putative regulation of glucose and lipid metabolism by IL-4.
Methods:
C57BL/6 mice were intraperitoneally injected with either adenovirus containing full-length IL-4 encoding gene (AdIL-4) or recombinant IL-4 for mimicking the status of transient and long-term IL-4 overexpression, respectively, and the effects of the overexpressed IL-4 to glucose/lipid metabolism and insulin sensitivity were subsequently investigated.
Results:
Our results reveal that IL-4 improves insulin sensitivity and glucose tolerance through upregulating Akt phosphorylation while attenuating GSK-3β activities. IL-4 is also involved in lipid metabolism by inhibiting lipid accumulation in fat tissues, which lead to decreased weight gain and fat mass.
Conclusions:
Our results suggest that IL-4 regulates glucose and lipid metabolism by promoting insulin sensitivity, glucose tolerance and inhibiting lipid deposits. This study uncovers the novel roles of IL-4 in metabolism and provides new insights in the interaction between cytokines/immune responses, insulin sensitivity and metabolism.</description><subject>Adenoviruses</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Glucose - metabolism</subject><subject>Complications and side effects</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Epidemiology</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Gene Expression Regulation - genetics</subject><subject>Genetic aspects</subject><subject>Glucose</subject><subject>Glucose metabolism</subject><subject>Glucose Tolerance Test</subject><subject>Glycogen Synthase Kinase 3 - metabolism</subject><subject>Glycogen Synthase Kinase 3 beta</subject><subject>Health Promotion and Disease Prevention</subject><subject>Humans</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Insulin Resistance - genetics</subject><subject>Interleukin-4</subject><subject>Interleukin-4 - metabolism</subject><subject>Internal Medicine</subject><subject>Laboratory animals</subject><subject>Lipid metabolism</subject><subject>Lipid Metabolism - genetics</subject><subject>Lipids</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Obesity</subject><subject>Obesity - metabolism</subject><subject>original-article</subject><subject>Phosphorylation</subject><subject>Physiological aspects</subject><subject>Public Health</subject><subject>Risk factors</subject><issn>0307-0565</issn><issn>1476-5497</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpt0dtrFDEUB-Agil2rbz7LgCg-OGsyuczMYyneoFAQfQ6ZzJlt1kyy5lLY_96Mu9atlPMQSL6cXH4IvSR4TTDtPpitXzeYkDUR3SO0IqwVNWd9-xitMMVtjbngZ-hZjFuMMee4eYrOGtL1jAi8QtffYJOtSsa7yk_VxmbtI1TW7MxYzZDU4K2Jc6XcWBkXszWuiuCiSebWpH017Mt0gmAh_zSuZs_Rk0nZCC-O4zn68enj98sv9dX156-XF1e15gSnmqhejZ1qaSsGwkcuhNA9GaHRFE-KNGTiGAvOlW6BTKRlHWe0F0QApd1AB3qO3h367oL_lSEmOZuowVrlwOcoCW4Ya7vyzEJf_0e3PgdXbvdHleqaE7VRFqRxk09B6aWpvGj6FjNMiShq_YAqNcJstHcwmTJ_b8Pbkw03oGy6id7m5cPjffj-AHXwMQaY5C6YWYV9uaRcgpYlaLkELUvQhb86PioPM4x3-G-yBbw5AhW1slNQTpv4z4nSk-HF1QcXy5LbQDj9nQcPrg7eqZQD3DUsaDEL-Q1IWMY-</recordid><startdate>20120701</startdate><enddate>20120701</enddate><creator>Chang, Y-H</creator><creator>Ho, K-T</creator><creator>Lu, S-H</creator><creator>Huang, C-N</creator><creator>Shiau, M-Y</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>IQODW</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>3V.</scope><scope>7T2</scope><scope>7TK</scope><scope>7TS</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20120701</creationdate><title>Regulation of glucose lipid metabolism and insulin sensitivity by interleukin-4</title><author>Chang, Y-H ; Ho, K-T ; Lu, S-H ; Huang, C-N ; Shiau, M-Y</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c510t-1a9ad8a7376b15d5666c91de2c30fa121f500655ac7e1f17485439616e338b3b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adenoviruses</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Glucose - metabolism</topic><topic>Complications and side effects</topic><topic>Cytokines</topic><topic>Diabetes</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Epidemiology</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Gene Expression Regulation - genetics</topic><topic>Genetic aspects</topic><topic>Glucose</topic><topic>Glucose metabolism</topic><topic>Glucose Tolerance Test</topic><topic>Glycogen Synthase Kinase 3 - metabolism</topic><topic>Glycogen Synthase Kinase 3 beta</topic><topic>Health Promotion and Disease Prevention</topic><topic>Humans</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Insulin Resistance - genetics</topic><topic>Interleukin-4</topic><topic>Interleukin-4 - metabolism</topic><topic>Internal Medicine</topic><topic>Laboratory animals</topic><topic>Lipid metabolism</topic><topic>Lipid Metabolism - genetics</topic><topic>Lipids</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Obesity</topic><topic>Obesity - metabolism</topic><topic>original-article</topic><topic>Phosphorylation</topic><topic>Physiological aspects</topic><topic>Public Health</topic><topic>Risk factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chang, Y-H</creatorcontrib><creatorcontrib>Ho, K-T</creatorcontrib><creatorcontrib>Lu, S-H</creatorcontrib><creatorcontrib>Huang, C-N</creatorcontrib><creatorcontrib>Shiau, M-Y</creatorcontrib><collection>Pascal-Francis</collection><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>Health and Safety Science Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database (ProQuest)</collection><collection>Biological Science 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>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>International Journal of Obesity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chang, Y-H</au><au>Ho, K-T</au><au>Lu, S-H</au><au>Huang, C-N</au><au>Shiau, M-Y</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of glucose lipid metabolism and insulin sensitivity by interleukin-4</atitle><jtitle>International Journal of Obesity</jtitle><stitle>Int J Obes</stitle><addtitle>Int J Obes (Lond)</addtitle><date>2012-07-01</date><risdate>2012</risdate><volume>36</volume><issue>7</issue><spage>993</spage><epage>998</epage><pages>993-998</pages><issn>0307-0565</issn><eissn>1476-5497</eissn><coden>IJOBDP</coden><abstract>Objective:
Abundant evidence has demonstrated that long-term cytokine-mediated inflammation is a risk factor for obesity and type 2 diabetes mellitus (T2DM). Our previous study reveals a significant association between promoter polymorphisms of Th2-derived cytokine interleukin-4 (IL-4) and T2DM, which suggests possible roles of IL-4 in metabolism. In this study, we focused on examining the putative regulation of glucose and lipid metabolism by IL-4.
Methods:
C57BL/6 mice were intraperitoneally injected with either adenovirus containing full-length IL-4 encoding gene (AdIL-4) or recombinant IL-4 for mimicking the status of transient and long-term IL-4 overexpression, respectively, and the effects of the overexpressed IL-4 to glucose/lipid metabolism and insulin sensitivity were subsequently investigated.
Results:
Our results reveal that IL-4 improves insulin sensitivity and glucose tolerance through upregulating Akt phosphorylation while attenuating GSK-3β activities. IL-4 is also involved in lipid metabolism by inhibiting lipid accumulation in fat tissues, which lead to decreased weight gain and fat mass.
Conclusions:
Our results suggest that IL-4 regulates glucose and lipid metabolism by promoting insulin sensitivity, glucose tolerance and inhibiting lipid deposits. This study uncovers the novel roles of IL-4 in metabolism and provides new insights in the interaction between cytokines/immune responses, insulin sensitivity and metabolism.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>21894160</pmid><doi>10.1038/ijo.2011.168</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | International Journal of Obesity, 2012-07, Vol.36 (7), p.993-998 |
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| source | MEDLINE; Nature Journals Online; EZB-FREE-00999 freely available EZB journals; SpringerLink Journals - AutoHoldings |
| subjects | Adenoviruses Animals Biological and medical sciences Blood Glucose - metabolism Complications and side effects Cytokines Diabetes Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Epidemiology Etiopathogenesis. Screening. Investigations. Target tissue resistance Gene Expression Regulation - genetics Genetic aspects Glucose Glucose metabolism Glucose Tolerance Test Glycogen Synthase Kinase 3 - metabolism Glycogen Synthase Kinase 3 beta Health Promotion and Disease Prevention Humans Insulin Insulin resistance Insulin Resistance - genetics Interleukin-4 Interleukin-4 - metabolism Internal Medicine Laboratory animals Lipid metabolism Lipid Metabolism - genetics Lipids Medical sciences Medicine Medicine & Public Health Metabolic Diseases Metabolism Mice Mice, Inbred C57BL Obesity Obesity - metabolism original-article Phosphorylation Physiological aspects Public Health Risk factors |
| title | Regulation of glucose lipid metabolism and insulin sensitivity by interleukin-4 |
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