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Titolo:
REDUCED AMYLIN RELEASE IS A CHARACTERISTIC OF IMPAIRED GLUCOSE-TOLERANCE AND TYPE-2 DIABETES IN JAPANESE-AMERICANS
Autore:
KAHN SE; VERCHERE CB; ANDRIKOPOULOS S; ASBERRY PJ; LEONETTI DL; WAHL PW; BOYKO EJ; SCHWARTZ RS; NEWELLMORRIS L; FUJIMOTO WY;
Indirizzi:
VA PUGET SOUND HLTH CARE SYST 151,1660 S COLUMBIAN WAY SEATTLE WA 98108 UNIV WASHINGTON,DEPT MED,DEPT ANTHROPOL,DIV METAB ENDOCRINOL & NUTR SEATTLE WA 98195 UNIV WASHINGTON,DEPT MED,DEPT ANTHROPOL,DIV GEN INTERNAL MED SEATTLE WA 98195 UNIV WASHINGTON,DEPT MED,DEPT ANTHROPOL,DIV GERONTOL & GERIATR MED SEATTLE WA 98195 UNIV WASHINGTON,DEPT BIOSTAT SEATTLE WA 98195
Titolo Testata:
Diabetes
fascicolo: 4, volume: 47, anno: 1998,
pagine: 640 - 645
SICI:
0012-1797(1998)47:4<640:RARIAC>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
ISLET AMYLOID POLYPEPTIDE; TRANSGENIC MICE; INSULIN-SECRETION; BETA-CELLS; PANCREATIC-ISLETS; PIMA-INDIANS; C-PEPTIDE; A-CELLS; B-CELLS; MELLITUS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
43
Recensione:
Indirizzi per estratti:
Citazione:
S.E. Kahn et al., "REDUCED AMYLIN RELEASE IS A CHARACTERISTIC OF IMPAIRED GLUCOSE-TOLERANCE AND TYPE-2 DIABETES IN JAPANESE-AMERICANS", Diabetes, 47(4), 1998, pp. 640-645

Abstract

Islet amyloid is a characteristic feature of type 2 diabetes. Its major component is the normal beta-cell secretory product amylin, or islet amyloid polypeptide (IAPP). To determine whether increased or disproportionate release of amylin may explain the propensity for amyloid deposition in type 2 diabetes, we measured plasma amylin-like immunoreactivity (ALI) and immunoreactive insulin (IRI) release in response to an oral glucose load in 94 Japanese-American subjects with normal glucose tolerance (NGT; n = 56), impaired glucose tolerance (IGT; n = 10), and type 2 diabetes (n = 28) as defined by World Health Organization criteria. The incremental increase In AI,I, IRI, and glucose (G) at 30 min after oral glucose ingestion was used to calculate Delta ALI/DeltaG and Delta IRI/Delta G as measures of beta-cell function. Overall glucose metabolism was assessed as the incremental glucose area (glucoseAUG) during the 2 h of the oral glucose tolerance test. As expected, plasma glucose concentrations at both fasting (NGT, 5.0 +/- 0.4; IGT, 5.5 +/- 0.1; type 2 diabetes, 6.2 +/- 0.3 mmol/l; P < 0.0001) and 2 h (NGT, 6.7 +/- 0.1; IGT, 9.4 +/- 0.3; type 2 diabetes, 13.2 +/- 0.5 mmol/l; P < 0.0001) were elevated in individuals with IGT and type 2 diabetes. In response to glucose ingestion, plasma IRI and ALI increased in all subjects, but these increments were lower in individuals with reduced glucose tolerance, as reflected in the Delta IRI/Delta G (NGT, 119 +/- 10.3; IGT, 60.7 +/- 7.1; type 2 diabetes, 49.7 +/- 5.4 pmol/l; P < 0.0001) and Delta ALI/Delta G (NGT, 2.6 +/- 0.2; IGT, 1.8 +/- 0.3;type 2 diabetes, 1.2 +/- 0.1 pmol/l; P < 0.0001). Moreover, these reductions in the 30-min incremental ALI and IRI responses were proportionate such that the molar ratio of ALI to IRI was not different among the three groups (NGT, 2.6 +/- 0.2; IGT, 2.9 +/- 0.3; type 2 diabetes, 2.9 +/- 0.3%; NS). Further, the relationship between beta-cell function, measured as either Delta IRI/Delta G or Delta ALI/Delta G, and glucose metabolism, assessed as glucose AUG, was nonlinear and inverse in nature, with r(2) values of 0.38 (P < 0.0001) and 0.33 (P < 0.0001), respectively. We conclude that the reduced beta-cell function of IGT and type 2 diabetes includes proportionate reductions in both IRI and ALI release. Thus, it is unlikely that the development of islet amyloid in type 2 diabetes is the result of increased release of ALI.

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Documento generato il 05/12/20 alle ore 10:37:35