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Evidence for the homeostatic regulation of induced beta cell mass expansion
Diabetes results from an insufficient insulin-secreting beta cell mass. Restoration of beta cell mass through pharmaceutically induced endogenous beta cell mass expansion may revolutionise diabetes therapy. However, it remains to be determined whether the induced beta cell mass expansion is under ho...
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| Published in: | Diabetologia 2006-12, Vol.49 (12), p.2910-2919 |
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| container_end_page | 2919 |
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| container_title | Diabetologia |
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| creator | LIPSETT, M. A AUSTIN, E. B CASTELLARIN, M. L LEMAY, J ROSENBERG, L |
| description | Diabetes results from an insufficient insulin-secreting beta cell mass. Restoration of beta cell mass through pharmaceutically induced endogenous beta cell mass expansion may revolutionise diabetes therapy. However, it remains to be determined whether the induced beta cell mass expansion is under homeostatic regulation.
Beta cell mass expansion rates were derived from three separate studies of continuous stimulation of islet neogenesis, including the partial duct obstruction of euglycaemic Syrian hamsters, administration of a pentadecapeptide with the same amino acid sequence as residues 104-118 of islet neogenesis-associated protein (INGAP(104-118)) to euglycaemic Syrian hamsters, as well as to euglycaemic CD-1 mice. The incidence of islet neogenesis, average beta cell size, and beta cell replication and apoptotic rates were determined.
Partial duct obstruction led to a approximately 2.5-fold increase in endocrine tissue at day 56 (p |
| doi_str_mv | 10.1007/s00125-006-0428-8 |
| format | article |
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Beta cell mass expansion rates were derived from three separate studies of continuous stimulation of islet neogenesis, including the partial duct obstruction of euglycaemic Syrian hamsters, administration of a pentadecapeptide with the same amino acid sequence as residues 104-118 of islet neogenesis-associated protein (INGAP(104-118)) to euglycaemic Syrian hamsters, as well as to euglycaemic CD-1 mice. The incidence of islet neogenesis, average beta cell size, and beta cell replication and apoptotic rates were determined.
Partial duct obstruction led to a approximately 2.5-fold increase in endocrine tissue at day 56 (p<0.05). From day 0 to day 7 the average rate of change of islet area was 12.7% per day, and this rate decreased to 5.3% per day from day 7 to day 42, and to 2.8% per day from day 42 to day 56. Administration of INGAP(104-118) to adult hamsters led to a 31% increase in total beta cell mass at day 30 (p=0.031). From day 0 to day 10 the average rate of beta cell mass expansion was 148 mug/day, whereas from day 10 to day 30 it decreased to 45 mug/day. INGAP(104-118) administration to adult CD-1 mice resulted in an approximately twofold increase in beta cell mass after 31 days (p=0.021). However, at day 90, there was no significant difference vs age-matched control mice (p=0.30), even though the neogenic beta cell mass was approximately fourfold greater (p=0.026). Beta cell replication was decreased by 56% (p<0.048), whereas beta cell apoptosis was fourfold greater (p<0.003) in 90-day INGAP(104-118)-treated mice compared with age-matched control mice.
These data indicate that in the presence of ongoing islet neogenesis, homeostatic regulatory mechanisms intervene to regulate beta cell mass according to the prevailing metabolic requirements.</description><identifier>ISSN: 0012-186X</identifier><identifier>EISSN: 1432-0428</identifier><identifier>DOI: 10.1007/s00125-006-0428-8</identifier><identifier>PMID: 17096119</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Animals ; Apoptosis ; Biological and medical sciences ; Blood & organ donations ; Blood Glucose - metabolism ; Cell Division ; Cell Size ; Cricetinae ; Diabetes ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Female ; Hibernation ; Homeostasis ; Hypotheses ; Insulin ; Insulin - analysis ; Insulin-Secreting Cells - cytology ; Insulin-Secreting Cells - physiology ; Laboratories ; Male ; Medical sciences ; Mesocricetus ; Metabolism ; Ostomy ; Pancreas ; Pancreatic Ducts - physiology ; Pancreatitis-Associated Proteins ; Proteins</subject><ispartof>Diabetologia, 2006-12, Vol.49 (12), p.2910-2919</ispartof><rights>2007 INIST-CNRS</rights><rights>Springer-Verlag 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c399t-423d4427008b1930e4b9db52613aec92d76adc3391209f71198c72ae7c915a403</citedby><cites>FETCH-LOGICAL-c399t-423d4427008b1930e4b9db52613aec92d76adc3391209f71198c72ae7c915a403</cites></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=18299726$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17096119$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LIPSETT, M. A</creatorcontrib><creatorcontrib>AUSTIN, E. B</creatorcontrib><creatorcontrib>CASTELLARIN, M. L</creatorcontrib><creatorcontrib>LEMAY, J</creatorcontrib><creatorcontrib>ROSENBERG, L</creatorcontrib><title>Evidence for the homeostatic regulation of induced beta cell mass expansion</title><title>Diabetologia</title><addtitle>Diabetologia</addtitle><description>Diabetes results from an insufficient insulin-secreting beta cell mass. Restoration of beta cell mass through pharmaceutically induced endogenous beta cell mass expansion may revolutionise diabetes therapy. However, it remains to be determined whether the induced beta cell mass expansion is under homeostatic regulation.
Beta cell mass expansion rates were derived from three separate studies of continuous stimulation of islet neogenesis, including the partial duct obstruction of euglycaemic Syrian hamsters, administration of a pentadecapeptide with the same amino acid sequence as residues 104-118 of islet neogenesis-associated protein (INGAP(104-118)) to euglycaemic Syrian hamsters, as well as to euglycaemic CD-1 mice. The incidence of islet neogenesis, average beta cell size, and beta cell replication and apoptotic rates were determined.
Partial duct obstruction led to a approximately 2.5-fold increase in endocrine tissue at day 56 (p<0.05). From day 0 to day 7 the average rate of change of islet area was 12.7% per day, and this rate decreased to 5.3% per day from day 7 to day 42, and to 2.8% per day from day 42 to day 56. Administration of INGAP(104-118) to adult hamsters led to a 31% increase in total beta cell mass at day 30 (p=0.031). From day 0 to day 10 the average rate of beta cell mass expansion was 148 mug/day, whereas from day 10 to day 30 it decreased to 45 mug/day. INGAP(104-118) administration to adult CD-1 mice resulted in an approximately twofold increase in beta cell mass after 31 days (p=0.021). However, at day 90, there was no significant difference vs age-matched control mice (p=0.30), even though the neogenic beta cell mass was approximately fourfold greater (p=0.026). Beta cell replication was decreased by 56% (p<0.048), whereas beta cell apoptosis was fourfold greater (p<0.003) in 90-day INGAP(104-118)-treated mice compared with age-matched control mice.
These data indicate that in the presence of ongoing islet neogenesis, homeostatic regulatory mechanisms intervene to regulate beta cell mass according to the prevailing metabolic requirements.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Blood & organ donations</subject><subject>Blood Glucose - metabolism</subject><subject>Cell Division</subject><subject>Cell Size</subject><subject>Cricetinae</subject><subject>Diabetes</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Female</subject><subject>Hibernation</subject><subject>Homeostasis</subject><subject>Hypotheses</subject><subject>Insulin</subject><subject>Insulin - analysis</subject><subject>Insulin-Secreting Cells - cytology</subject><subject>Insulin-Secreting Cells - physiology</subject><subject>Laboratories</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mesocricetus</subject><subject>Metabolism</subject><subject>Ostomy</subject><subject>Pancreas</subject><subject>Pancreatic Ducts - physiology</subject><subject>Pancreatitis-Associated Proteins</subject><subject>Proteins</subject><issn>0012-186X</issn><issn>1432-0428</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><recordid>eNpdkE1r3DAQhkVoSDZpf0AvRRSSm9vRh_VxLCFfNJBLCr0JWR5nHWxrK9kl_ffVZhcWcpoZ5pnh5SHkM4NvDEB_zwCM1xWAqkByU5kjsmJS8LfpA1lt1xUz6vcpOcv5BQBELdUJOWUarGLMrsjP6799i1NA2sVE5zXSdRwx5tnPfaAJn5ehdHGisaP91C4BW9rg7GnAYaCjz5ni68ZPuTAfyXHnh4yf9vWc_Lq5frq6qx4eb--vfjxUQVg7V5KLVkquAUzDrACUjW2bmismPAbLW618G4SwjIPtdIlpguYedbCs9hLEObnc_d2k-GfBPLuxz9s8fsK4ZKcME7aWtoBf34EvcUlTyeY4E0Zqq-oCsR0UUsw5Yec2qR99-ucYuK1mt9Psima3FetMufmyf7w0I7aHi73XAlzsAZ-DH7rkp9DnA2e4tZor8R98GoNi</recordid><startdate>20061201</startdate><enddate>20061201</enddate><creator>LIPSETT, M. 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Target tissue resistance</topic><topic>Female</topic><topic>Hibernation</topic><topic>Homeostasis</topic><topic>Hypotheses</topic><topic>Insulin</topic><topic>Insulin - analysis</topic><topic>Insulin-Secreting Cells - cytology</topic><topic>Insulin-Secreting Cells - physiology</topic><topic>Laboratories</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mesocricetus</topic><topic>Metabolism</topic><topic>Ostomy</topic><topic>Pancreas</topic><topic>Pancreatic Ducts - physiology</topic><topic>Pancreatitis-Associated Proteins</topic><topic>Proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LIPSETT, M. A</creatorcontrib><creatorcontrib>AUSTIN, E. B</creatorcontrib><creatorcontrib>CASTELLARIN, M. 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A</au><au>AUSTIN, E. B</au><au>CASTELLARIN, M. L</au><au>LEMAY, J</au><au>ROSENBERG, L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Evidence for the homeostatic regulation of induced beta cell mass expansion</atitle><jtitle>Diabetologia</jtitle><addtitle>Diabetologia</addtitle><date>2006-12-01</date><risdate>2006</risdate><volume>49</volume><issue>12</issue><spage>2910</spage><epage>2919</epage><pages>2910-2919</pages><issn>0012-186X</issn><eissn>1432-0428</eissn><abstract>Diabetes results from an insufficient insulin-secreting beta cell mass. Restoration of beta cell mass through pharmaceutically induced endogenous beta cell mass expansion may revolutionise diabetes therapy. However, it remains to be determined whether the induced beta cell mass expansion is under homeostatic regulation.
Beta cell mass expansion rates were derived from three separate studies of continuous stimulation of islet neogenesis, including the partial duct obstruction of euglycaemic Syrian hamsters, administration of a pentadecapeptide with the same amino acid sequence as residues 104-118 of islet neogenesis-associated protein (INGAP(104-118)) to euglycaemic Syrian hamsters, as well as to euglycaemic CD-1 mice. The incidence of islet neogenesis, average beta cell size, and beta cell replication and apoptotic rates were determined.
Partial duct obstruction led to a approximately 2.5-fold increase in endocrine tissue at day 56 (p<0.05). From day 0 to day 7 the average rate of change of islet area was 12.7% per day, and this rate decreased to 5.3% per day from day 7 to day 42, and to 2.8% per day from day 42 to day 56. Administration of INGAP(104-118) to adult hamsters led to a 31% increase in total beta cell mass at day 30 (p=0.031). From day 0 to day 10 the average rate of beta cell mass expansion was 148 mug/day, whereas from day 10 to day 30 it decreased to 45 mug/day. INGAP(104-118) administration to adult CD-1 mice resulted in an approximately twofold increase in beta cell mass after 31 days (p=0.021). However, at day 90, there was no significant difference vs age-matched control mice (p=0.30), even though the neogenic beta cell mass was approximately fourfold greater (p=0.026). Beta cell replication was decreased by 56% (p<0.048), whereas beta cell apoptosis was fourfold greater (p<0.003) in 90-day INGAP(104-118)-treated mice compared with age-matched control mice.
These data indicate that in the presence of ongoing islet neogenesis, homeostatic regulatory mechanisms intervene to regulate beta cell mass according to the prevailing metabolic requirements.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>17096119</pmid><doi>10.1007/s00125-006-0428-8</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Apoptosis Biological and medical sciences Blood & organ donations Blood Glucose - metabolism Cell Division Cell Size Cricetinae Diabetes Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Hibernation Homeostasis Hypotheses Insulin Insulin - analysis Insulin-Secreting Cells - cytology Insulin-Secreting Cells - physiology Laboratories Male Medical sciences Mesocricetus Metabolism Ostomy Pancreas Pancreatic Ducts - physiology Pancreatitis-Associated Proteins Proteins |
| title | Evidence for the homeostatic regulation of induced beta cell mass expansion |
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