Source:http://linkedlifedata.com/resource/pubmed/id/11108273
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
2000-12-6
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pubmed:abstractText |
Glucose homeostasis in mammals is maintained by insulin secretion from the beta-cells of the islets of Langerhans. Type 2 diabetes results either from primary beta-cell failure alone and/or a failure to secrete enough insulin to overcome insulin resistance. Here, we show that continuous infusion of glucagon-like peptide-1 (7-36) (GLP-1; an insulinotropic agent), to young and old animals, had effects on the beta-cell of the pancreas other than simply on the insulin secretory apparatus. Our previous studies on a rodent model of glucose intolerance, the aging Wistar rat, show that a plateau in islet size, insulin content, and beta-cell mass is reached at 13 months, despite a continuing increase in body weight. Continuous sc infusion of GLP-1 (1.5 pM/kg x min), over 5 days, resulted in normal glucose tolerance. Our current results in both young and old rats demonstrate that treatment caused an up-regulation of pancreatic-duodenum homeobox-1 (PDX-1) expression in islets and total pancreas, induced pancreatic cell proliferation, and beta-cell neogenesis. The effects on levels of PDX-1 messenger RNA were abrogated by simultaneous infusion of Exendin (9-39), a specific antagonist of GLP-1. PDX-1 protein levels increased 4-fold in whole pancreata and 6-fold in islets in response to treatment. Beta-cell mass increased to 7.2 +/- 0.58 from 4.88 +/- 0.38 mg, treated vs. control, respectively, P < 0.02. Total pancreatic insulin content also increased from 0.55 +/- 0.02 to 1.32 +/- 0.11 microg/mg total pancreatic protein. Therefore, GLP-1 would seem to be a unique therapy that can stimulate pancreatic cell proliferation and beta-cell differentiation in the pancreas of rodents.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Blood Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Glucagon,
http://linkedlifedata.com/resource/pubmed/chemical/Glucagon-Like Peptide 1,
http://linkedlifedata.com/resource/pubmed/chemical/Homeodomain Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Precursors,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators,
http://linkedlifedata.com/resource/pubmed/chemical/pancreatic and duodenal homeobox 1...
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0013-7227
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
141
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4600-5
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:11108273-Aging,
pubmed-meshheading:11108273-Animals,
pubmed-meshheading:11108273-Blood Glucose,
pubmed-meshheading:11108273-Cell Division,
pubmed-meshheading:11108273-Gene Expression Regulation,
pubmed-meshheading:11108273-Glucagon,
pubmed-meshheading:11108273-Glucagon-Like Peptide 1,
pubmed-meshheading:11108273-Glucose Intolerance,
pubmed-meshheading:11108273-Homeodomain Proteins,
pubmed-meshheading:11108273-Insulin,
pubmed-meshheading:11108273-Islets of Langerhans,
pubmed-meshheading:11108273-Pancreas,
pubmed-meshheading:11108273-Peptide Fragments,
pubmed-meshheading:11108273-Protein Precursors,
pubmed-meshheading:11108273-Rats,
pubmed-meshheading:11108273-Rats, Wistar,
pubmed-meshheading:11108273-Trans-Activators
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pubmed:year |
2000
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pubmed:articleTitle |
Glucagon-like peptide-1 induces cell proliferation and pancreatic-duodenum homeobox-1 expression and increases endocrine cell mass in the pancreas of old, glucose-intolerant rats.
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pubmed:affiliation |
Cedars-Sinai Medical Center, Division of Endocrinology, Los Angeles, California 90048, USA.
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pubmed:publicationType |
Journal Article
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