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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
1998-4-7
|
| pubmed:abstractText |
To define the mechanisms involved in the evolution of diabetes in the Zucker diabetic fatty (ZDF) rat, beta-cell mass and replication rates were determined by immunochemistry, point-counting morphometry, and 6-h 5-bromo-2'-deoxyuridine (BrdU) incorporation. The beta-cell mass in 5- to 7-week-old prediabetic ZDF rats (4.3 +/- 0.06 mg) was similar to age-matched insulin-resistant Zucker fatty (ZF) rats (3.7 +/- 0.05 mg) and greater than that in Zucker lean control (ZLC) rats (1.9 +/- 0.3, P < 0.05). At 12 weeks (after diabetes onset), beta-cell mass in the ZDF rats (8.1 +/- 1.7 mg) was significantly lower than the ZF rats (15.7 +/- 1.8 mg). The mass in the ZF rats was significantly greater than in the ZLC rats (4.3 +/- 0.8 mg, P < 0.05). The beta-cell proliferation rate (mean of both time points) was significantly greater in the ZDF rats (0.88 +/- 0.1%) compared with the ZF and ZLC rats (0.53 +/- 0.07%, 0.62 +/- 0.07%, respectively, P < 0.05), yet ZDF rats have a lower beta-cell mass than the ZF rats despite a higher proliferative rate. Morphological evidence of neogenesis and apoptosis is evident in the ZF and ZDF rats. In addition, even at 5-7 weeks a modest defect in insulin secretion per beta-cell unit was found by pancreas perfusion. These studies provide evidence that the expansion of beta-cell mass in response to insulin resistance and insulin secretory defects in diabetic ZDF rats is inadequate. This failure of beta-cell mass expansion in the ZDF rat does not appear to be from a reduction in the rate of beta-cell proliferation or neogenesis, suggesting an increased rate of cell death by apoptosis.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Glucagon,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Pancreatic Polypeptide,
http://linkedlifedata.com/resource/pubmed/chemical/Somatostatin
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
0012-1797
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
47
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
358-64
|
| pubmed:dateRevised |
2011-11-17
|
| pubmed:meshHeading |
pubmed-meshheading:9519740-Animals,
pubmed-meshheading:9519740-Apoptosis,
pubmed-meshheading:9519740-Cohort Studies,
pubmed-meshheading:9519740-Diabetes Mellitus, Type 2,
pubmed-meshheading:9519740-Disease Models, Animal,
pubmed-meshheading:9519740-Dose-Response Relationship, Drug,
pubmed-meshheading:9519740-Glucagon,
pubmed-meshheading:9519740-Glucose,
pubmed-meshheading:9519740-Glucose Intolerance,
pubmed-meshheading:9519740-Glucose Tolerance Test,
pubmed-meshheading:9519740-Immunohistochemistry,
pubmed-meshheading:9519740-Insulin,
pubmed-meshheading:9519740-Insulin Resistance,
pubmed-meshheading:9519740-Islets of Langerhans,
pubmed-meshheading:9519740-Male,
pubmed-meshheading:9519740-Pancreatic Polypeptide,
pubmed-meshheading:9519740-Perfusion,
pubmed-meshheading:9519740-Rats,
pubmed-meshheading:9519740-Rats, Zucker,
pubmed-meshheading:9519740-Somatostatin,
pubmed-meshheading:9519740-Time Factors
|
| pubmed:year |
1998
|
| pubmed:articleTitle |
Role of apoptosis in failure of beta-cell mass compensation for insulin resistance and beta-cell defects in the male Zucker diabetic fatty rat.
|
| pubmed:affiliation |
Department of Medicine, The University of Chicago and Pritzker School of Medicine, Illinois 60637, USA.
|
| pubmed:publicationType |
Journal Article,
Comparative Study,
In Vitro,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|