Central GLP-2 Enhances Hepatic Insulin Sensitivity via Activating PI3K Signaling in POMC Neurons
Glucagon-like peptides (GLP-1/GLP-2) are coproduced and highlighted as key modulators to improve glucose homeostasis and insulin sensitivity after bariatric surgery. However, it is unknown if CNS GLP-2 plays any physiological role in the control of glucose homeostasis and insulin sensitivity. We sho...
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| Veröffentlicht in: | Cell metabolism 2013-07, Vol.18 (1), p.86-98 |
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| creator | Shi, Xuemei Zhou, Fuguo Li, Xiaojie Chang, Benny Li, Depei Wang, Yi Tong, Qingchun Xu, Yong Fukuda, Makoto Zhao, Jean J. Li, Defa Burrin, Douglas G. Chan, Lawrence Guan, Xinfu |
| description | Glucagon-like peptides (GLP-1/GLP-2) are coproduced and highlighted as key modulators to improve glucose homeostasis and insulin sensitivity after bariatric surgery. However, it is unknown if CNS GLP-2 plays any physiological role in the control of glucose homeostasis and insulin sensitivity. We show that mice lacking GLP-2 receptor (GLP-2R) in POMC neurons display glucose intolerance and hepatic insulin resistance. GLP-2R activation in POMC neurons is required for GLP-2 to enhance insulin-mediated suppression of hepatic glucose production (HGP) and gluconeogenesis. GLP-2 directly modulates excitability of POMC neurons in GLP-2R- and PI3K-dependent manners. GLP-2 initiates GLP-2R-p85α interaction and facilitates PI3K-Akt-dependent FoxO1 nuclear exclusion in POMC neurons. Central GLP-2 suppresses basal HGP and enhances insulin sensitivity, which are abolished in POMC-p110α KO mice. Thus, CNS GLP-2 plays a key physiological role in the control of HGP through activating PI3K-dependent modulation of membrane excitability and nuclear transcription of POMC neurons in the brain.
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•GLP-2R in POMC neurons is required for GLP-2 to promote glucose homeostasis•GLP-2 modulates excitability of POMC neurons in GLP-2R- and PI3K-dependent manners•GLP-2 activates GLP-2R-PI3K-FoxO1 signaling pathway in POMC neurons•Central GLP-2 enhances hepatic insulin sensitivity in a PI3K-dependent manner |
| doi_str_mv | 10.1016/j.cmet.2013.06.014 |
| format | Article |
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[Display omitted]
•GLP-2R in POMC neurons is required for GLP-2 to promote glucose homeostasis•GLP-2 modulates excitability of POMC neurons in GLP-2R- and PI3K-dependent manners•GLP-2 activates GLP-2R-PI3K-FoxO1 signaling pathway in POMC neurons•Central GLP-2 enhances hepatic insulin sensitivity in a PI3K-dependent manner</description><identifier>ISSN: 1550-4131</identifier><identifier>EISSN: 1932-7420</identifier><identifier>DOI: 10.1016/j.cmet.2013.06.014</identifier><identifier>PMID: 23823479</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; bariatric surgery ; brain ; Cells, Cultured ; Forkhead Box Protein O1 ; Forkhead Transcription Factors - physiology ; Glucagon-Like Peptide 2 - physiology ; Glucagon-Like Peptide-2 Receptor ; glucagon-like peptides ; gluconeogenesis ; glucose ; Glucose - metabolism ; glycemic control ; homeostasis ; Homeostasis - physiology ; insulin resistance ; Insulin Resistance - physiology ; Liver - physiology ; Male ; Mice ; Mice, Inbred Strains ; Mice, Knockout ; Models, Animal ; neurons ; Neurons - cytology ; Neurons - physiology ; phosphatidylinositol 3-kinase ; Phosphatidylinositol 3-Kinases - physiology ; Pro-Opiomelanocortin - deficiency ; Pro-Opiomelanocortin - genetics ; Pro-Opiomelanocortin - physiology ; Proto-Oncogene Proteins c-akt - physiology ; Receptors, Glucagon - deficiency ; Receptors, Glucagon - genetics ; Receptors, Glucagon - physiology ; Signal Transduction - physiology</subject><ispartof>Cell metabolism, 2013-07, Vol.18 (1), p.86-98</ispartof><rights>2013 Elsevier Inc.</rights><rights>Copyright © 2013 Elsevier Inc. All rights reserved.</rights><rights>2013 Elsevier Inc. All rights reserved. 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c554t-26c79a4034f942a46e6fd6dcaded83ae61ef588f769757a14f5b1658551a202a3</citedby><cites>FETCH-LOGICAL-c554t-26c79a4034f942a46e6fd6dcaded83ae61ef588f769757a14f5b1658551a202a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1550413113002581$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23823479$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shi, Xuemei</creatorcontrib><creatorcontrib>Zhou, Fuguo</creatorcontrib><creatorcontrib>Li, Xiaojie</creatorcontrib><creatorcontrib>Chang, Benny</creatorcontrib><creatorcontrib>Li, Depei</creatorcontrib><creatorcontrib>Wang, Yi</creatorcontrib><creatorcontrib>Tong, Qingchun</creatorcontrib><creatorcontrib>Xu, Yong</creatorcontrib><creatorcontrib>Fukuda, Makoto</creatorcontrib><creatorcontrib>Zhao, Jean J.</creatorcontrib><creatorcontrib>Li, Defa</creatorcontrib><creatorcontrib>Burrin, Douglas G.</creatorcontrib><creatorcontrib>Chan, Lawrence</creatorcontrib><creatorcontrib>Guan, Xinfu</creatorcontrib><title>Central GLP-2 Enhances Hepatic Insulin Sensitivity via Activating PI3K Signaling in POMC Neurons</title><title>Cell metabolism</title><addtitle>Cell Metab</addtitle><description>Glucagon-like peptides (GLP-1/GLP-2) are coproduced and highlighted as key modulators to improve glucose homeostasis and insulin sensitivity after bariatric surgery. However, it is unknown if CNS GLP-2 plays any physiological role in the control of glucose homeostasis and insulin sensitivity. We show that mice lacking GLP-2 receptor (GLP-2R) in POMC neurons display glucose intolerance and hepatic insulin resistance. GLP-2R activation in POMC neurons is required for GLP-2 to enhance insulin-mediated suppression of hepatic glucose production (HGP) and gluconeogenesis. GLP-2 directly modulates excitability of POMC neurons in GLP-2R- and PI3K-dependent manners. GLP-2 initiates GLP-2R-p85α interaction and facilitates PI3K-Akt-dependent FoxO1 nuclear exclusion in POMC neurons. Central GLP-2 suppresses basal HGP and enhances insulin sensitivity, which are abolished in POMC-p110α KO mice. Thus, CNS GLP-2 plays a key physiological role in the control of HGP through activating PI3K-dependent modulation of membrane excitability and nuclear transcription of POMC neurons in the brain.
[Display omitted]
•GLP-2R in POMC neurons is required for GLP-2 to promote glucose homeostasis•GLP-2 modulates excitability of POMC neurons in GLP-2R- and PI3K-dependent manners•GLP-2 activates GLP-2R-PI3K-FoxO1 signaling pathway in POMC neurons•Central GLP-2 enhances hepatic insulin sensitivity in a PI3K-dependent manner</description><subject>Animals</subject><subject>bariatric surgery</subject><subject>brain</subject><subject>Cells, Cultured</subject><subject>Forkhead Box Protein O1</subject><subject>Forkhead Transcription Factors - physiology</subject><subject>Glucagon-Like Peptide 2 - physiology</subject><subject>Glucagon-Like Peptide-2 Receptor</subject><subject>glucagon-like peptides</subject><subject>gluconeogenesis</subject><subject>glucose</subject><subject>Glucose - metabolism</subject><subject>glycemic control</subject><subject>homeostasis</subject><subject>Homeostasis - physiology</subject><subject>insulin resistance</subject><subject>Insulin Resistance - physiology</subject><subject>Liver - physiology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred Strains</subject><subject>Mice, Knockout</subject><subject>Models, Animal</subject><subject>neurons</subject><subject>Neurons - cytology</subject><subject>Neurons - physiology</subject><subject>phosphatidylinositol 3-kinase</subject><subject>Phosphatidylinositol 3-Kinases - physiology</subject><subject>Pro-Opiomelanocortin - deficiency</subject><subject>Pro-Opiomelanocortin - genetics</subject><subject>Pro-Opiomelanocortin - physiology</subject><subject>Proto-Oncogene Proteins c-akt - physiology</subject><subject>Receptors, Glucagon - deficiency</subject><subject>Receptors, Glucagon - genetics</subject><subject>Receptors, Glucagon - physiology</subject><subject>Signal Transduction - physiology</subject><issn>1550-4131</issn><issn>1932-7420</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1r3DAQhkVpSdKkf6CHomMvdvUtG0IgLPlYum0Wkp5VRR5vtHjljWQv5N9HZpPQXtqTNOiZlxk9CH2mpKSEqm_r0m1gKBmhvCSqJFS8Q0e05qzQgpH3-S4lKQTl9BB9TGlNCFe85gfokPGKcaHrI_R7BmGItsNXi2XB8EV4sMFBwtewtYN3eB7S2PmAbyEkP_idH57wzlt87nKRibDCyzn_jm_9KthuKjO8vPkxwz9hjH1IJ-hDa7sEn17OY_Tr8uJudl0sbq7ms_NF4aQUQ8GU07UVhIu2FswKBaptVONsA03FLSgKrayqVqtaS22paOU9VbKSklpGmOXH6Gyfux3vN9C4_VpmG_3GxifTW2_-fgn-waz6neFaMqpYDvj6EhD7xxHSYDY-Oeg6G6Afk6GacymlZtX_UV5XgjFNJ5TtURf7lCK0bxNRYiaLZm0mi2ayaIgy2WJu-vLnLm8tr9oycLoHIP_ozkM0yXnI4hofwQ2m6f2_8p8BrGStkA</recordid><startdate>20130702</startdate><enddate>20130702</enddate><creator>Shi, Xuemei</creator><creator>Zhou, Fuguo</creator><creator>Li, Xiaojie</creator><creator>Chang, Benny</creator><creator>Li, Depei</creator><creator>Wang, Yi</creator><creator>Tong, Qingchun</creator><creator>Xu, Yong</creator><creator>Fukuda, Makoto</creator><creator>Zhao, Jean J.</creator><creator>Li, Defa</creator><creator>Burrin, Douglas G.</creator><creator>Chan, Lawrence</creator><creator>Guan, Xinfu</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</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>7X8</scope><scope>7S9</scope><scope>L.6</scope><scope>5PM</scope></search><sort><creationdate>20130702</creationdate><title>Central GLP-2 Enhances Hepatic Insulin Sensitivity via Activating PI3K Signaling in POMC Neurons</title><author>Shi, Xuemei ; Zhou, Fuguo ; Li, Xiaojie ; Chang, Benny ; Li, Depei ; Wang, Yi ; Tong, Qingchun ; Xu, Yong ; Fukuda, Makoto ; Zhao, Jean J. ; Li, Defa ; Burrin, Douglas G. ; Chan, Lawrence ; Guan, Xinfu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c554t-26c79a4034f942a46e6fd6dcaded83ae61ef588f769757a14f5b1658551a202a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>bariatric surgery</topic><topic>brain</topic><topic>Cells, Cultured</topic><topic>Forkhead Box Protein O1</topic><topic>Forkhead Transcription Factors - physiology</topic><topic>Glucagon-Like Peptide 2 - physiology</topic><topic>Glucagon-Like Peptide-2 Receptor</topic><topic>glucagon-like peptides</topic><topic>gluconeogenesis</topic><topic>glucose</topic><topic>Glucose - metabolism</topic><topic>glycemic control</topic><topic>homeostasis</topic><topic>Homeostasis - physiology</topic><topic>insulin resistance</topic><topic>Insulin Resistance - physiology</topic><topic>Liver - physiology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred Strains</topic><topic>Mice, Knockout</topic><topic>Models, Animal</topic><topic>neurons</topic><topic>Neurons - cytology</topic><topic>Neurons - physiology</topic><topic>phosphatidylinositol 3-kinase</topic><topic>Phosphatidylinositol 3-Kinases - physiology</topic><topic>Pro-Opiomelanocortin - deficiency</topic><topic>Pro-Opiomelanocortin - genetics</topic><topic>Pro-Opiomelanocortin - physiology</topic><topic>Proto-Oncogene Proteins c-akt - physiology</topic><topic>Receptors, Glucagon - deficiency</topic><topic>Receptors, Glucagon - genetics</topic><topic>Receptors, Glucagon - physiology</topic><topic>Signal Transduction - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shi, Xuemei</creatorcontrib><creatorcontrib>Zhou, Fuguo</creatorcontrib><creatorcontrib>Li, Xiaojie</creatorcontrib><creatorcontrib>Chang, Benny</creatorcontrib><creatorcontrib>Li, Depei</creatorcontrib><creatorcontrib>Wang, Yi</creatorcontrib><creatorcontrib>Tong, Qingchun</creatorcontrib><creatorcontrib>Xu, Yong</creatorcontrib><creatorcontrib>Fukuda, Makoto</creatorcontrib><creatorcontrib>Zhao, Jean J.</creatorcontrib><creatorcontrib>Li, Defa</creatorcontrib><creatorcontrib>Burrin, Douglas G.</creatorcontrib><creatorcontrib>Chan, Lawrence</creatorcontrib><creatorcontrib>Guan, Xinfu</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shi, Xuemei</au><au>Zhou, Fuguo</au><au>Li, Xiaojie</au><au>Chang, Benny</au><au>Li, Depei</au><au>Wang, Yi</au><au>Tong, Qingchun</au><au>Xu, Yong</au><au>Fukuda, Makoto</au><au>Zhao, Jean J.</au><au>Li, Defa</au><au>Burrin, Douglas G.</au><au>Chan, Lawrence</au><au>Guan, Xinfu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Central GLP-2 Enhances Hepatic Insulin Sensitivity via Activating PI3K Signaling in POMC Neurons</atitle><jtitle>Cell metabolism</jtitle><addtitle>Cell Metab</addtitle><date>2013-07-02</date><risdate>2013</risdate><volume>18</volume><issue>1</issue><spage>86</spage><epage>98</epage><pages>86-98</pages><issn>1550-4131</issn><eissn>1932-7420</eissn><abstract>Glucagon-like peptides (GLP-1/GLP-2) are coproduced and highlighted as key modulators to improve glucose homeostasis and insulin sensitivity after bariatric surgery. However, it is unknown if CNS GLP-2 plays any physiological role in the control of glucose homeostasis and insulin sensitivity. We show that mice lacking GLP-2 receptor (GLP-2R) in POMC neurons display glucose intolerance and hepatic insulin resistance. GLP-2R activation in POMC neurons is required for GLP-2 to enhance insulin-mediated suppression of hepatic glucose production (HGP) and gluconeogenesis. GLP-2 directly modulates excitability of POMC neurons in GLP-2R- and PI3K-dependent manners. GLP-2 initiates GLP-2R-p85α interaction and facilitates PI3K-Akt-dependent FoxO1 nuclear exclusion in POMC neurons. Central GLP-2 suppresses basal HGP and enhances insulin sensitivity, which are abolished in POMC-p110α KO mice. Thus, CNS GLP-2 plays a key physiological role in the control of HGP through activating PI3K-dependent modulation of membrane excitability and nuclear transcription of POMC neurons in the brain.
[Display omitted]
•GLP-2R in POMC neurons is required for GLP-2 to promote glucose homeostasis•GLP-2 modulates excitability of POMC neurons in GLP-2R- and PI3K-dependent manners•GLP-2 activates GLP-2R-PI3K-FoxO1 signaling pathway in POMC neurons•Central GLP-2 enhances hepatic insulin sensitivity in a PI3K-dependent manner</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>23823479</pmid><doi>10.1016/j.cmet.2013.06.014</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals bariatric surgery brain Cells, Cultured Forkhead Box Protein O1 Forkhead Transcription Factors - physiology Glucagon-Like Peptide 2 - physiology Glucagon-Like Peptide-2 Receptor glucagon-like peptides gluconeogenesis glucose Glucose - metabolism glycemic control homeostasis Homeostasis - physiology insulin resistance Insulin Resistance - physiology Liver - physiology Male Mice Mice, Inbred Strains Mice, Knockout Models, Animal neurons Neurons - cytology Neurons - physiology phosphatidylinositol 3-kinase Phosphatidylinositol 3-Kinases - physiology Pro-Opiomelanocortin - deficiency Pro-Opiomelanocortin - genetics Pro-Opiomelanocortin - physiology Proto-Oncogene Proteins c-akt - physiology Receptors, Glucagon - deficiency Receptors, Glucagon - genetics Receptors, Glucagon - physiology Signal Transduction - physiology |
| title | Central GLP-2 Enhances Hepatic Insulin Sensitivity via Activating PI3K Signaling in POMC Neurons |
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