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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3 Pt 1
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pubmed:dateCreated |
1993-11-23
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pubmed:abstractText |
To determine if increased secretion of amylin can be implicated in the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM) in vitro and in vivo, we studied its relationships to insulin in insulin-resistant rats with and without NIDDM. In obesity-associated and dexamethasone-induced insulin resistance without diabetes, basal and stimulated secretion of amylin and insulin by isolated pancreata were proportionately elevated, leaving the amylin-to-insulin ratio (A/I) unchanged. By contrast, whenever diabetes occurred in dexamethasone-treated rats or in spontaneously diabetic obese insulin-resistant ZDF-drt male rats, a doubling of A/I was invariably observed due to an increase in amylin without a proportional increase in insulin secretion. Correction of dexamethasone-induced hyperglycemia with the glucocorticord receptor antagonist RU-486 was accompanied by a decline in A/I. Longitudinal in vivo studies demonstrated in both spontaneous and dexamethasone-induced models of NIDDM an increase in plasma A/I at the onset of hyperglycemia. In dexamethasone-induced diabetes, the increased A/I was associated with a high proamylin mRNA relative to proinsulin mRNA. We conclude that amylin and insulin expression and secretion rise in concert in compensated insulin-resistant states, but when hyperglycemia is present the increase in amylin exceeds that of insulin. Although a role of an increased A/I in the pathogenesis of NIDDM has not been established directly, these studies indicate that such a role could be possible.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Amyloid,
http://linkedlifedata.com/resource/pubmed/chemical/Dexamethasone,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Islet Amyloid Polypeptide,
http://linkedlifedata.com/resource/pubmed/chemical/Mifepristone,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Glucocorticoid,
http://linkedlifedata.com/resource/pubmed/chemical/Somatostatin
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
265
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
E446-53
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:8105694-Amyloid,
pubmed-meshheading:8105694-Animals,
pubmed-meshheading:8105694-Dexamethasone,
pubmed-meshheading:8105694-Diabetes Mellitus, Type 2,
pubmed-meshheading:8105694-Hyperglycemia,
pubmed-meshheading:8105694-Insulin,
pubmed-meshheading:8105694-Insulin Resistance,
pubmed-meshheading:8105694-Islet Amyloid Polypeptide,
pubmed-meshheading:8105694-Male,
pubmed-meshheading:8105694-Mifepristone,
pubmed-meshheading:8105694-Obesity,
pubmed-meshheading:8105694-Pancreas,
pubmed-meshheading:8105694-RNA, Messenger,
pubmed-meshheading:8105694-Rats,
pubmed-meshheading:8105694-Rats, Wistar,
pubmed-meshheading:8105694-Rats, Zucker,
pubmed-meshheading:8105694-Receptors, Glucocorticoid,
pubmed-meshheading:8105694-Somatostatin
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pubmed:year |
1993
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pubmed:articleTitle |
Amylin-insulin relationships in insulin resistance with and without diabetic hyperglycemia.
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pubmed:affiliation |
Gifford Laboratories, Department of Internal Medicine, University of Texas Southwestern Medical Center at Dallas 75235.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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