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Titolo:
GLUCOSE POTENTIATION OF ARGININE-INDUCED INSULIN-SECRETION IS IMPAIRED IN SUBJECTS WITH A GLUCOKINASE GLU258LYS MUTATION
Autore:
WAJNGOT A; ALVARSSON M; GLASER A; EFENDIC S; LUTHMAN H; GRILL V;
Indirizzi:
KAROLINSKA HOSP,DEPT ENDOCRINOL S-17176 STOCKHOLM SWEDEN KAROLINSKA HOSP,DEPT ENDOCRINOL S-17176 STOCKHOLM SWEDEN KAROLINSKA HOSP,DEPT CLIN GENET S-10401 STOCKHOLM SWEDEN
Titolo Testata:
Diabetes
fascicolo: 12, volume: 43, anno: 1994,
pagine: 1402 - 1406
SICI:
0012-1797(1994)43:12<1402:GPOAII>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
DEPENDENT DIABETES-MELLITUS; BETA-CELL FUNCTION; GENE; SENSITIVITY; RESPONSES; CAPACITY; LINKAGE; YOUNG; CLAMP;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
31
Recensione:
Indirizzi per estratti:
Citazione:
A. Wajngot et al., "GLUCOSE POTENTIATION OF ARGININE-INDUCED INSULIN-SECRETION IS IMPAIRED IN SUBJECTS WITH A GLUCOKINASE GLU258LYS MUTATION", Diabetes, 43(12), 1994, pp. 1402-1406

Abstract

Insulin and glucagon release and insulin sensitivity were investigated in patients with glucokinase deficiency. Five subjects with a missense mutation (Glu256Lys) were studied. They were compared with six healthy subjects with low insulin response but normal glucose tolerance. Insulin and glucagon levels were measured at blood glucose 7.1 +/- 0.1 mmol/l and at 10.9 +/- 0.2 mmol/l with or without arginine (5 g i.v.). Insulin sensitivity was assessed as the ratio between infused glucoseand the insulin level (M:I) during hyperglycemic clamps. Glu256Lys subjects were nonobese and had fasting blood glucose 6.7 +/- 0.1 mmol/l (P < 0.001 vs. control group). Insulin release was reduced in responseto 11 mmol/l glucose (61% of control group, P < 0.05) as well as to arginine in the presence of 11 mmol/l glucose (54% of control group, P < 0.01). Also, the slope of potentiation, i.e., the enhancement of arginine-induced release as a function of prevailing glucose concentration, was reduced (Delta insulin/Delta glucose, 47% of control group, P <0.05). As for glucagon release, the response to arginine was not inhibited normally by glucose, resulting in threefold higher levels at 11 mmol/l glucose versus control subjects. Insulin sensitivity, assessed as M:I, was significantly (P < 0.05) reduced (55% of control group). Glucokinase deficiency thus affects not only insulin responses to glucose per se but also glucose potentiation of responses to non-nutrient secretagogues. Abnormalities in glucagon release and insulin sensitivity coexist with attenuated insulin responses in glucokinase-deficient subjects.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 06:34:41