Ontogeny of Regeneration of β-Cells in the Neonatal Rat after Treatment with Streptozotocin
We induced partial β-cell loss within the pancreas of neonatal rats using streptozotocin (STZ) to better characterize the mechanisms leading to β-cell regeneration postnatally. Rats were administered either STZ (70 mg/kg) or buffer alone on postnatal d 4, and the endocrine pancreas was examined betw...
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| Veröffentlicht in: | Endocrinology (Philadelphia) 2006-05, Vol.147 (5), p.2346-2356 |
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| description | We induced partial β-cell loss within the pancreas of neonatal rats using streptozotocin (STZ) to better characterize the mechanisms leading to β-cell regeneration postnatally. Rats were administered either STZ (70 mg/kg) or buffer alone on postnatal d 4, and the endocrine pancreas was examined between 4 and 40 d later. STZ-treated rats showed an approximately 60% loss of existing β-cells and a moderate hyperglycemia ( |
| doi_str_mv | 10.1210/en.2005-0396 |
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J</creator><creatorcontrib>Thyssen, Sandra ; Arany, Edith ; Hill, D. J</creatorcontrib><description>We induced partial β-cell loss within the pancreas of neonatal rats using streptozotocin (STZ) to better characterize the mechanisms leading to β-cell regeneration postnatally. Rats were administered either STZ (70 mg/kg) or buffer alone on postnatal d 4, and the endocrine pancreas was examined between 4 and 40 d later. STZ-treated rats showed an approximately 60% loss of existing β-cells and a moderate hyperglycemia (<15 mm glucose), with levels returning to near-control values after 20 d. Within preexisting islets, there was increased cell proliferation in both insulin- and glucagon-positive cells at 8 d as well as α-cell hyperplasia. These were associated with increased pancreatic content and circulating levels of glucagon. Pancreatic levels of glucagon-like polypeptide-1 (GLP-1) were increased 8 d after STZ compared with control values, and the GLP-1/glucagon ratio changed in favor of GLP-1. Administration of a GLP-1 receptor antagonist, GLP-1-(9–39), resulted in decreased recovery of β-cells after STZ and worse glucose tolerance. Atypical glucagon-positive cells were found within islets that colocalized pancreatic duodenal homeobox-1 or glucose transporter-2. Pancreatic levels of insulin mRNA did not return to control values until 40 d after STZ. Insulin-positive cells were found after 8 d that colocalized glucagon and GLP-1. The model shows that the pancreas of the young rat can rapidly regenerate a loss of β-cells, and this is associated with hyperplasia of α-cells with an altered phenotype of increased GLP-1 synthesis. The target cells of GLP-1 probably include immature β-cells that coexpress proglucagon.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2005-0396</identifier><identifier>PMID: 16484329</identifier><identifier>CODEN: ENDOAO</identifier><language>eng</language><publisher>Bethesda, MD: Endocrine Society</publisher><subject>Animals ; Animals, Newborn ; Beta cells ; Biological and medical sciences ; Cell Proliferation ; DNA Primers - chemistry ; Female ; Fundamental and applied biological sciences. Psychology ; Glucagon ; Glucagon - chemistry ; Glucagon - metabolism ; Glucose ; Glucose - metabolism ; Glucose tolerance ; Glucose transporter ; Homeobox ; Hyperglycemia ; Hyperplasia ; Immunohistochemistry ; Insulin ; Insulin - metabolism ; Insulin-Secreting Cells - physiology ; Islets of Langerhans - metabolism ; Male ; Mice ; Microscopy, Fluorescence ; mRNA ; Neonates ; Ontogeny ; Pancreas ; Pancreas - metabolism ; Phenotypes ; Polypeptides ; Proglucagon - metabolism ; Radioimmunoassay ; Rats ; Rats, Wistar ; Regeneration ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - metabolism ; Streptozocin ; Streptozocin - pharmacology ; Time Factors ; Vertebrates: endocrinology</subject><ispartof>Endocrinology (Philadelphia), 2006-05, Vol.147 (5), p.2346-2356</ispartof><rights>Copyright © 2006 by The Endocrine Society 2006</rights><rights>2006 INIST-CNRS</rights><rights>Copyright © 2006 by The Endocrine Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c461t-e8106f3c7358c88ded97c2453c9b2ce22c72f221efa81acc546dbb1cb2c8cdc83</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17712246$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16484329$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Thyssen, Sandra</creatorcontrib><creatorcontrib>Arany, Edith</creatorcontrib><creatorcontrib>Hill, D. J</creatorcontrib><title>Ontogeny of Regeneration of β-Cells in the Neonatal Rat after Treatment with Streptozotocin</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>We induced partial β-cell loss within the pancreas of neonatal rats using streptozotocin (STZ) to better characterize the mechanisms leading to β-cell regeneration postnatally. Rats were administered either STZ (70 mg/kg) or buffer alone on postnatal d 4, and the endocrine pancreas was examined between 4 and 40 d later. STZ-treated rats showed an approximately 60% loss of existing β-cells and a moderate hyperglycemia (<15 mm glucose), with levels returning to near-control values after 20 d. Within preexisting islets, there was increased cell proliferation in both insulin- and glucagon-positive cells at 8 d as well as α-cell hyperplasia. These were associated with increased pancreatic content and circulating levels of glucagon. Pancreatic levels of glucagon-like polypeptide-1 (GLP-1) were increased 8 d after STZ compared with control values, and the GLP-1/glucagon ratio changed in favor of GLP-1. Administration of a GLP-1 receptor antagonist, GLP-1-(9–39), resulted in decreased recovery of β-cells after STZ and worse glucose tolerance. Atypical glucagon-positive cells were found within islets that colocalized pancreatic duodenal homeobox-1 or glucose transporter-2. Pancreatic levels of insulin mRNA did not return to control values until 40 d after STZ. Insulin-positive cells were found after 8 d that colocalized glucagon and GLP-1. The model shows that the pancreas of the young rat can rapidly regenerate a loss of β-cells, and this is associated with hyperplasia of α-cells with an altered phenotype of increased GLP-1 synthesis. The target cells of GLP-1 probably include immature β-cells that coexpress proglucagon.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Beta cells</subject><subject>Biological and medical sciences</subject><subject>Cell Proliferation</subject><subject>DNA Primers - chemistry</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glucagon</subject><subject>Glucagon - chemistry</subject><subject>Glucagon - metabolism</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Glucose tolerance</subject><subject>Glucose transporter</subject><subject>Homeobox</subject><subject>Hyperglycemia</subject><subject>Hyperplasia</subject><subject>Immunohistochemistry</subject><subject>Insulin</subject><subject>Insulin - metabolism</subject><subject>Insulin-Secreting Cells - physiology</subject><subject>Islets of Langerhans - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Microscopy, Fluorescence</subject><subject>mRNA</subject><subject>Neonates</subject><subject>Ontogeny</subject><subject>Pancreas</subject><subject>Pancreas - metabolism</subject><subject>Phenotypes</subject><subject>Polypeptides</subject><subject>Proglucagon - metabolism</subject><subject>Radioimmunoassay</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Regeneration</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - metabolism</subject><subject>Streptozocin</subject><subject>Streptozocin - pharmacology</subject><subject>Time Factors</subject><subject>Vertebrates: endocrinology</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kM2KFTEQhYMoznV051oCom7sMX_dSS_l4h8MDozjTgi51dVOD32TniSNjI_lg_hMprkNF0RXVUV9nDp1CHnK2RkXnL1BfyYYqysm2-Ye2fBW1ZXmmt0nG8a4rLQQ-oQ8SummjEop-ZCc8EYZJUW7Id8ufA7f0d_R0NNLLB1Gl4fgl_n3r2qL45jo4Gm-RvoZg3fZjfTSZer6jJFeRXR5jz7TH0O-pl9yxCmHnyEHGPxj8qB3Y8Inaz0lX9-_u9p-rM4vPnzavj2vQDU8V2g4a3oJWtYGjOmwazUIVUtodwJQCNCiF4Jj7wx3ALVqut2OQ1ka6MDIU_LyoDvFcDtjynY_JCjOnccwJ9to02jOdAGf_wXehDn64s1KLlmtC7PIvT5QEENKEXs7xWHv4p3lzC6ZW_R2ydwumRf82So67_bYHeE15AK8WAGXwI19dB6GdOS05kKoRejVgQvz9L-T1XpSHkj0XYA4eJwipnT85p9G_wDSv6dE</recordid><startdate>20060501</startdate><enddate>20060501</enddate><creator>Thyssen, Sandra</creator><creator>Arany, Edith</creator><creator>Hill, D. 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J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c461t-e8106f3c7358c88ded97c2453c9b2ce22c72f221efa81acc546dbb1cb2c8cdc83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Beta cells</topic><topic>Biological and medical sciences</topic><topic>Cell Proliferation</topic><topic>DNA Primers - chemistry</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glucagon</topic><topic>Glucagon - chemistry</topic><topic>Glucagon - metabolism</topic><topic>Glucose</topic><topic>Glucose - metabolism</topic><topic>Glucose tolerance</topic><topic>Glucose transporter</topic><topic>Homeobox</topic><topic>Hyperglycemia</topic><topic>Hyperplasia</topic><topic>Immunohistochemistry</topic><topic>Insulin</topic><topic>Insulin - metabolism</topic><topic>Insulin-Secreting Cells - physiology</topic><topic>Islets of Langerhans - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Microscopy, Fluorescence</topic><topic>mRNA</topic><topic>Neonates</topic><topic>Ontogeny</topic><topic>Pancreas</topic><topic>Pancreas - metabolism</topic><topic>Phenotypes</topic><topic>Polypeptides</topic><topic>Proglucagon - metabolism</topic><topic>Radioimmunoassay</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Regeneration</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - metabolism</topic><topic>Streptozocin</topic><topic>Streptozocin - pharmacology</topic><topic>Time Factors</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Thyssen, Sandra</creatorcontrib><creatorcontrib>Arany, Edith</creatorcontrib><creatorcontrib>Hill, D. 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J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ontogeny of Regeneration of β-Cells in the Neonatal Rat after Treatment with Streptozotocin</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2006-05-01</date><risdate>2006</risdate><volume>147</volume><issue>5</issue><spage>2346</spage><epage>2356</epage><pages>2346-2356</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><coden>ENDOAO</coden><abstract>We induced partial β-cell loss within the pancreas of neonatal rats using streptozotocin (STZ) to better characterize the mechanisms leading to β-cell regeneration postnatally. Rats were administered either STZ (70 mg/kg) or buffer alone on postnatal d 4, and the endocrine pancreas was examined between 4 and 40 d later. STZ-treated rats showed an approximately 60% loss of existing β-cells and a moderate hyperglycemia (<15 mm glucose), with levels returning to near-control values after 20 d. Within preexisting islets, there was increased cell proliferation in both insulin- and glucagon-positive cells at 8 d as well as α-cell hyperplasia. These were associated with increased pancreatic content and circulating levels of glucagon. Pancreatic levels of glucagon-like polypeptide-1 (GLP-1) were increased 8 d after STZ compared with control values, and the GLP-1/glucagon ratio changed in favor of GLP-1. Administration of a GLP-1 receptor antagonist, GLP-1-(9–39), resulted in decreased recovery of β-cells after STZ and worse glucose tolerance. Atypical glucagon-positive cells were found within islets that colocalized pancreatic duodenal homeobox-1 or glucose transporter-2. Pancreatic levels of insulin mRNA did not return to control values until 40 d after STZ. Insulin-positive cells were found after 8 d that colocalized glucagon and GLP-1. The model shows that the pancreas of the young rat can rapidly regenerate a loss of β-cells, and this is associated with hyperplasia of α-cells with an altered phenotype of increased GLP-1 synthesis. The target cells of GLP-1 probably include immature β-cells that coexpress proglucagon.</abstract><cop>Bethesda, MD</cop><pub>Endocrine Society</pub><pmid>16484329</pmid><doi>10.1210/en.2005-0396</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Animals, Newborn Beta cells Biological and medical sciences Cell Proliferation DNA Primers - chemistry Female Fundamental and applied biological sciences. Psychology Glucagon Glucagon - chemistry Glucagon - metabolism Glucose Glucose - metabolism Glucose tolerance Glucose transporter Homeobox Hyperglycemia Hyperplasia Immunohistochemistry Insulin Insulin - metabolism Insulin-Secreting Cells - physiology Islets of Langerhans - metabolism Male Mice Microscopy, Fluorescence mRNA Neonates Ontogeny Pancreas Pancreas - metabolism Phenotypes Polypeptides Proglucagon - metabolism Radioimmunoassay Rats Rats, Wistar Regeneration Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - metabolism Streptozocin Streptozocin - pharmacology Time Factors Vertebrates: endocrinology |
| title | Ontogeny of Regeneration of β-Cells in the Neonatal Rat after Treatment with Streptozotocin |
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