Lower Blood Glucose, Hyperglucagonemia, and Pancreatic α Cell Hyperplasia in Glucagon Receptor Knockout Mice
Glucagon, the counter-regulatory hormone to insulin, is secreted from pancreatic α cells in response to low blood glucose. To examine the role of glucagon in glucose homeostasis, mice were generated with a null mutation of the glucagon receptor (Gcgr-/-). These mice display lower blood glucose level...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2003-02, Vol.100 (3), p.1438-1443 |
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| creator | Gelling, R. W. Du, X. Q. Dichmann, D. S. Rømer, J. Huang, H. Cui, L. Obici, S. Tang, B. Holst, J. J. Fledelius, C. Johansen, P. B. Rossetti, L. Jelicks, L. A. Serup, P. Nishimura, E. Charron, M. J. |
| description | Glucagon, the counter-regulatory hormone to insulin, is secreted from pancreatic α cells in response to low blood glucose. To examine the role of glucagon in glucose homeostasis, mice were generated with a null mutation of the glucagon receptor (Gcgr-/-). These mice display lower blood glucose levels throughout the day and improved glucose tolerance but similar insulin levels compared with control animals. Gcgr-/-mice displayed supraphysiological glucagon levels associated with postnatal enlargement of the pancreas and hyperplasia of islets due predominantly to α cell, and to a lesser extent, δ cell proliferation. In addition, increased proglucagon expression and processing resulted in increased pancreatic glucogen-like peptide 1 (GLP-1) (1-37) and GLP-1 amide (1-36 amide) content and a 3- to 10-fold increase in circulating GLP-1 amide. Gcgr-/-mice also displayed reduced adiposity and leptin levels but normal body weight, food intake, and energy expenditure. These data indicate that glucagon is essential for maintenance of normal glycemia and postnatal regulation of islet and α and δ cell numbers. Furthermore, the lean phenotype of Gcgr-/-mice suggests glucagon action may be involved in the regulation of whole body composition. |
| doi_str_mv | 10.1073/pnas.0237106100 |
| format | Article |
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W. ; Du, X. Q. ; Dichmann, D. S. ; Rømer, J. ; Huang, H. ; Cui, L. ; Obici, S. ; Tang, B. ; Holst, J. J. ; Fledelius, C. ; Johansen, P. B. ; Rossetti, L. ; Jelicks, L. A. ; Serup, P. ; Nishimura, E. ; Charron, M. J.</creator><creatorcontrib>Gelling, R. W. ; Du, X. Q. ; Dichmann, D. S. ; Rømer, J. ; Huang, H. ; Cui, L. ; Obici, S. ; Tang, B. ; Holst, J. J. ; Fledelius, C. ; Johansen, P. B. ; Rossetti, L. ; Jelicks, L. A. ; Serup, P. ; Nishimura, E. ; Charron, M. J.</creatorcontrib><description>Glucagon, the counter-regulatory hormone to insulin, is secreted from pancreatic α cells in response to low blood glucose. To examine the role of glucagon in glucose homeostasis, mice were generated with a null mutation of the glucagon receptor (Gcgr-/-). These mice display lower blood glucose levels throughout the day and improved glucose tolerance but similar insulin levels compared with control animals. Gcgr-/-mice displayed supraphysiological glucagon levels associated with postnatal enlargement of the pancreas and hyperplasia of islets due predominantly to α cell, and to a lesser extent, δ cell proliferation. In addition, increased proglucagon expression and processing resulted in increased pancreatic glucogen-like peptide 1 (GLP-1) (1-37) and GLP-1 amide (1-36 amide) content and a 3- to 10-fold increase in circulating GLP-1 amide. Gcgr-/-mice also displayed reduced adiposity and leptin levels but normal body weight, food intake, and energy expenditure. These data indicate that glucagon is essential for maintenance of normal glycemia and postnatal regulation of islet and α and δ cell numbers. Furthermore, the lean phenotype of Gcgr-/-mice suggests glucagon action may be involved in the regulation of whole body composition.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.0237106100</identifier><identifier>PMID: 12552113</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Amides ; Animals ; Biological Sciences ; Blood Glucose - metabolism ; Body Weight ; Calorimetry ; Cell Division ; Cellular biology ; Cyclic AMP - metabolism ; Epididymis - metabolism ; Epinephrine - pharmacology ; Fasting ; Glucagon - blood ; Glucose ; Glucose - metabolism ; Hormones ; Hormones - metabolism ; Hyperplasia ; Immunohistochemistry ; Insulin ; Insulin - metabolism ; Islets of Langerhans - pathology ; Lean body mass ; Liver ; Liver - metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Microscopy, Fluorescence ; Pancreas ; Phenotype ; Receptors ; Receptors, Glucagon - genetics ; Receptors, Glucagon - physiology ; Rodents ; Time Factors</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2003-02, Vol.100 (3), p.1438-1443</ispartof><rights>Copyright 1993-2003 National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Feb 4, 2003</rights><rights>Copyright © 2003, The National Academy of Sciences 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c491t-2b67640ff812a73127dd59e4913e3a3ba5fa8c09eebc30aa865fefc9dd81c573</citedby><cites>FETCH-LOGICAL-c491t-2b67640ff812a73127dd59e4913e3a3ba5fa8c09eebc30aa865fefc9dd81c573</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/100/3.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/3138350$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/3138350$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,723,776,780,799,881,27901,27902,53766,53768,57992,58225</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12552113$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gelling, R. W.</creatorcontrib><creatorcontrib>Du, X. Q.</creatorcontrib><creatorcontrib>Dichmann, D. S.</creatorcontrib><creatorcontrib>Rømer, J.</creatorcontrib><creatorcontrib>Huang, H.</creatorcontrib><creatorcontrib>Cui, L.</creatorcontrib><creatorcontrib>Obici, S.</creatorcontrib><creatorcontrib>Tang, B.</creatorcontrib><creatorcontrib>Holst, J. J.</creatorcontrib><creatorcontrib>Fledelius, C.</creatorcontrib><creatorcontrib>Johansen, P. B.</creatorcontrib><creatorcontrib>Rossetti, L.</creatorcontrib><creatorcontrib>Jelicks, L. A.</creatorcontrib><creatorcontrib>Serup, P.</creatorcontrib><creatorcontrib>Nishimura, E.</creatorcontrib><creatorcontrib>Charron, M. J.</creatorcontrib><title>Lower Blood Glucose, Hyperglucagonemia, and Pancreatic α Cell Hyperplasia in Glucagon Receptor Knockout Mice</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Glucagon, the counter-regulatory hormone to insulin, is secreted from pancreatic α cells in response to low blood glucose. To examine the role of glucagon in glucose homeostasis, mice were generated with a null mutation of the glucagon receptor (Gcgr-/-). These mice display lower blood glucose levels throughout the day and improved glucose tolerance but similar insulin levels compared with control animals. Gcgr-/-mice displayed supraphysiological glucagon levels associated with postnatal enlargement of the pancreas and hyperplasia of islets due predominantly to α cell, and to a lesser extent, δ cell proliferation. In addition, increased proglucagon expression and processing resulted in increased pancreatic glucogen-like peptide 1 (GLP-1) (1-37) and GLP-1 amide (1-36 amide) content and a 3- to 10-fold increase in circulating GLP-1 amide. Gcgr-/-mice also displayed reduced adiposity and leptin levels but normal body weight, food intake, and energy expenditure. These data indicate that glucagon is essential for maintenance of normal glycemia and postnatal regulation of islet and α and δ cell numbers. Furthermore, the lean phenotype of Gcgr-/-mice suggests glucagon action may be involved in the regulation of whole body composition.</description><subject>Amides</subject><subject>Animals</subject><subject>Biological Sciences</subject><subject>Blood Glucose - metabolism</subject><subject>Body Weight</subject><subject>Calorimetry</subject><subject>Cell Division</subject><subject>Cellular biology</subject><subject>Cyclic AMP - metabolism</subject><subject>Epididymis - metabolism</subject><subject>Epinephrine - pharmacology</subject><subject>Fasting</subject><subject>Glucagon - blood</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Hormones</subject><subject>Hormones - metabolism</subject><subject>Hyperplasia</subject><subject>Immunohistochemistry</subject><subject>Insulin</subject><subject>Insulin - metabolism</subject><subject>Islets of Langerhans - pathology</subject><subject>Lean body mass</subject><subject>Liver</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microscopy, Fluorescence</subject><subject>Pancreas</subject><subject>Phenotype</subject><subject>Receptors</subject><subject>Receptors, Glucagon - genetics</subject><subject>Receptors, Glucagon - physiology</subject><subject>Rodents</subject><subject>Time Factors</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkcFu1DAURS0EosPAmg1CFouyadpnO4njBQs6ghYxCIS6tzzOy5AhsVM7AfpZ_AjfhIcZdQpiZVnv3Ov7fAl5yuCUgRRngzPxFLiQDEoGcI_MGCiWlbmC-2QGwGVW5Tw_Io9i3ACAKip4SI4YLwrOmJiRfum_Y6Dnnfc1vegm6yOe0MubAcM63czaO-xbc0KNq-kn42xAM7aW_vpJF9h1O3LoTGwNbd0fh62GfkaLw-gDfe-8_eqnkX5oLT4mDxrTRXyyP-fk6u2bq8Vltvx48W7xepnZXLEx46tSljk0TcW4kYJxWdeFwjQTKIxYmaIxlQWFuLICjKnKosHGqrqumC2kmJNXO9thWvVYW3RjMJ0eQtubcKO9afXfE9d-0Wv_TXNVyfTInBzv9cFfTxhH3bfRpnWNQz9FLblSVfruBL74B9z4Kbi0muaQYpdS8QSd7SAbfIwBm9sgDPS2Rb1tUR9aTIrnd_Mf-H1tCXi5B7bKgx1ooVkuKt1MXTfij_GO1f_JBDzbAZuY6rolBEuzAsRvfL28AQ</recordid><startdate>20030204</startdate><enddate>20030204</enddate><creator>Gelling, R. 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W.</au><au>Du, X. Q.</au><au>Dichmann, D. S.</au><au>Rømer, J.</au><au>Huang, H.</au><au>Cui, L.</au><au>Obici, S.</au><au>Tang, B.</au><au>Holst, J. J.</au><au>Fledelius, C.</au><au>Johansen, P. B.</au><au>Rossetti, L.</au><au>Jelicks, L. A.</au><au>Serup, P.</au><au>Nishimura, E.</au><au>Charron, M. J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lower Blood Glucose, Hyperglucagonemia, and Pancreatic α Cell Hyperplasia in Glucagon Receptor Knockout Mice</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2003-02-04</date><risdate>2003</risdate><volume>100</volume><issue>3</issue><spage>1438</spage><epage>1443</epage><pages>1438-1443</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>Glucagon, the counter-regulatory hormone to insulin, is secreted from pancreatic α cells in response to low blood glucose. To examine the role of glucagon in glucose homeostasis, mice were generated with a null mutation of the glucagon receptor (Gcgr-/-). These mice display lower blood glucose levels throughout the day and improved glucose tolerance but similar insulin levels compared with control animals. Gcgr-/-mice displayed supraphysiological glucagon levels associated with postnatal enlargement of the pancreas and hyperplasia of islets due predominantly to α cell, and to a lesser extent, δ cell proliferation. In addition, increased proglucagon expression and processing resulted in increased pancreatic glucogen-like peptide 1 (GLP-1) (1-37) and GLP-1 amide (1-36 amide) content and a 3- to 10-fold increase in circulating GLP-1 amide. Gcgr-/-mice also displayed reduced adiposity and leptin levels but normal body weight, food intake, and energy expenditure. These data indicate that glucagon is essential for maintenance of normal glycemia and postnatal regulation of islet and α and δ cell numbers. Furthermore, the lean phenotype of Gcgr-/-mice suggests glucagon action may be involved in the regulation of whole body composition.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>12552113</pmid><doi>10.1073/pnas.0237106100</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Amides Animals Biological Sciences Blood Glucose - metabolism Body Weight Calorimetry Cell Division Cellular biology Cyclic AMP - metabolism Epididymis - metabolism Epinephrine - pharmacology Fasting Glucagon - blood Glucose Glucose - metabolism Hormones Hormones - metabolism Hyperplasia Immunohistochemistry Insulin Insulin - metabolism Islets of Langerhans - pathology Lean body mass Liver Liver - metabolism Male Mice Mice, Inbred C57BL Microscopy, Fluorescence Pancreas Phenotype Receptors Receptors, Glucagon - genetics Receptors, Glucagon - physiology Rodents Time Factors |
| title | Lower Blood Glucose, Hyperglucagonemia, and Pancreatic α Cell Hyperplasia in Glucagon Receptor Knockout Mice |
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