Source:http://linkedlifedata.com/resource/pubmed/id/19819987
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
2009-11-25
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pubmed:abstractText |
Multiple bioactive peptides, including glucagon, glucagon-like peptide-1 (GLP-1), and GLP-2, are derived from the glucagon gene (Gcg). In the present study, we disrupted Gcg by introduction of GFP cDNA and established a knock-in mouse line. Gcg(gfp/gfp) mice that lack most, if not all, of Gcg-derived peptides were born in an expected Mendelian ratio without gross abnormalities. Gcg(gfp/gfp) mice showed lower blood glucose levels at 2 wk of age, but those in adult Gcg(gfp/gfp) mice were not significantly different from those in Gcg(+/+) and Gcg(gfp/+) mice, even after starvation for 16 h. Serum insulin levels in Gcg(gfp/gfp) mice were lower than in Gcg(+/+) and Gcg(gfp/+) on ad libitum feeding, but no significant differences were observed on starvation. Islet alpha-cells and intestinal L-cells were readily visualized in Gcg(gfp/gfp) and Gcg(gfp/+) mice under fluorescence. The Gcg(gfp/gfp) postnatally developed hyperplasia of islet alpha-cells, whereas the population of intestinal L-cells was not increased. In the Gcg(gfp/gfp), expression of Aristaless-related homeobox (Arx) was markedly increased in pancreas but not in intestine and suggested involvement of Arx in differential regulation of proliferation of Gcg-expressing cells. These results illustrated that Gcg-derived peptides are dispensable for survival and maintaining normoglycemia in adult mice and that Gcg-derived peptides differentially regulate proliferation/differentiation of alpha-cells and L-cells. The present model is useful for analyzing glucose/energy metabolism in the absence of Gcg-derived peptides. It is useful also for analysis of the development, differentiation, and function of Gcg-expressing cells, because such cells are readily visualized by fluorescence in this model.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1944-9917
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
23
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1990-9
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pubmed:meshHeading |
pubmed-meshheading:19819987-Animals,
pubmed-meshheading:19819987-Enteroendocrine Cells,
pubmed-meshheading:19819987-Flow Cytometry,
pubmed-meshheading:19819987-Gene Knock-In Techniques,
pubmed-meshheading:19819987-Genotype,
pubmed-meshheading:19819987-Glucagon,
pubmed-meshheading:19819987-Glucagon-Secreting Cells,
pubmed-meshheading:19819987-Hyperplasia,
pubmed-meshheading:19819987-Immunoenzyme Techniques,
pubmed-meshheading:19819987-Immunohistochemistry,
pubmed-meshheading:19819987-Islets of Langerhans,
pubmed-meshheading:19819987-Mice
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pubmed:year |
2009
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pubmed:articleTitle |
Mice deficient for glucagon gene-derived peptides display normoglycemia and hyperplasia of islet {alpha}-cells but not of intestinal L-cells.
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pubmed:affiliation |
Department of Genetics, Research Institute of Environmental Medicine, Nagoya University, Japan. hayashiy@riem.nagoya-u.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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