INTERRELATIONSHIP OF ISLET METABOLISM, ADENOSINE-TRIPHOSPHATE CONTENT AND INSULIN RELEASE
INTERRELATIONSHIP OF ISLET METABOLISM, ADENOSINE-TRIPHOSPHATE CONTENT AND INSULIN RELEASE
复制标题
DOI：
10.1042/bj1320223
复制
发表时间：
1973-01-01
影响因子：
4.1
通讯作者：
RANDLE, PJ
中科院分区：
文献类型：
--
作者：
ASHCROFT, SJ;WEERASINGHE, LC;RANDLE, PJ
The oxidation of some exogenous substrates and their effects on ATP content and insulin release in mouse pancreatic islets were measured. The ATP concentration of islets incubated without exogenous substrate shows a gradual decrease, which can be prevented by glucose or mannose (20mm) or leucine (2.5mm);d-glyceraldehyde (5mm) is as effective as glucose (5mm); fructose orN-acetylglucosamine (20mm), pyruvate (10mm) anddl-3-hydroxybutyrate (2mm) are less effective; galactose (20mm), acetate (10mm), octanoate (2mm) and succinate (10mm) have no ATP-maintaining ability. Islets oxidize glucose, mannose, glyceraldehyde, leucine and, less readily,N-acetylglucosamine and glucosamine; galactose, however, is poorly metabolized. Mannoheptulose inhibits the oxidation of glucose but not of glyceraldehyde. Insulin release, measured over a 2h incubation, is stimulated by glucose, mannose, leucine, glyceraldehyde or glucosamine but not by fructose orN-acetylglucosamine. The latter, however, potentiates the effects of glucose or glyceraldehyde (5mm) or leucine (2.5mm) on release; the potentiating effects are inhibited by mannoheptulose, which also blocks glucose-, but not glyceraldehyde- or leucine-stimulated release. In the presence of glucose (20mm), metabolic inhibitors depress insulin release and islet ATP content in parallel. However, rates of insulin release and ATP content measured after incubation with various combinations of exogenous substrates do not appear to be correlated. Sulphonylureas stimulate insulin release but decrease islet ATP concentrations. These results provide further evidence of a close association between the metabolic activity of exogenous substrates and their ability to initiate insulin release. Glucoreceptor models are formulated in the light of these observations and discussed.
