Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
Pieber, TR; Stein, DT; Ogawa, A; Alam, T; Ohneda, M; McCorkle, K; Chen, L; McGarry, JD; Unger, RH.
Amylin-insulin relationships in insulin resistance with and without diabetic hyperglycemia.
Am J Physiol. 1993; 265(3 Pt 1):E446-E453
Doi: 10.1152/ajpendo.1993.265.3.E446
Web of Science
PubMed
FullText
FullText_MUG
- Führende Autor*innen der Med Uni Graz
- Pieber Thomas
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- Abstract:
- 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.
- Find related publications in this database (using NLM MeSH Indexing)
- Amyloid - blood
- Amyloid - genetics
- Amyloid - secretion
- Animals -
- Dexamethasone - pharmacology
- Diabetes Mellitus, Type 2 - chemically induced
- Diabetes Mellitus, Type 2 - complications
- Diabetes Mellitus, Type 2 - genetics
- Hyperglycemia - etiology
- Hyperglycemia - physiopathology
- Insulin - blood
- Insulin - genetics
- Insulin - secretion
- Insulin Resistance -
- Islet Amyloid Polypeptide -
- Male -
- Mifepristone - pharmacology
- Obesity - genetics
- Obesity - physiopathology
- Pancreas - secretion
- RNA, Messenger - metabolism
- Rats -
- Rats, Wistar -
- Rats, Zucker -
- Receptors, Glucocorticoid - antagonists & inhibitors
- Somatostatin - metabolism
- Find related publications in this database (Keywords)
- MESSENGER RIBONUCLEIC ACID
- EXPRESSION
- SECRETION
- PANCREATIC PERFUSION
- PANCREAS
- OBESITY
- RAT
- ZUCKER
- ZDF DRT
- DEXAMETHASONE
- MIFEPRISTONE
- RU-486