Wege der Nachrichtenübermittlung bei der Stimulation der Sekretion von Insulin

Ammon, H. P. T.

doi:10.1002/pauz.19960250306

Cited by 2 publications

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“…It is possible that at least high glucose cannot produce its maximal possible secretory effect, because the insulin content is strongly reduced and since the insulin releasing capacity of glucose depends on islets insulin content [Steinke et al, 19721. As shown in Fig. 4 insulin secretion is initiated through depolarization and then modulated by glucose metabolism or by hormone actions (for review see Ammon, 1995): glucose by its metabolism first produces ATP and it is known that when the glucose concentration is raised the ATP!ADP ratio also increases. Elevation of the ATP/ADP ratio then closes ATPsensitive potassium channels, which leads to depolarization of the B-cell.…”

Section: Sensitization Of Insulin Secretionmentioning

confidence: 99%

Hyper- and hypoinsulinemia in type-2 diabetes: What may be wrong in the secretory mechanism of the B-cell

Ammon

2009

Exp Clin Endocrinol Diabetes

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Type-2 diabetes frequently is the consequence of overnutrition causing overweight, which then produces insulin resistance. The following hyperglycemia induces permanent overstimulation of the insulin secretory machinery of the B-cell, which results in hyperinsulinemia and/or hypoinsulinemia. The mechanisms, however, of these disturbances are not understood so far. Animal models, which can be used to solve these questions, are, among others, long-term incubation of pancreatic islets in culture in the presence of high glucose and/or long-term infusion of rats with glucose. Using these models sensitization [Bedoya and Jeanrenaud, 1991; Leahy et al., 1987; Purrello et al., 1992; Thams, 1991; Thibault et al., 1993; Timmers et al., 1990] and/or desensitization of insulin release [Bedoya and Jeanrenaud, 1991; Leahy et al., 1987; Davalli et al., 1992; Eizirik et al., 1992; Bolaffi et al., 1988; Timmers et al., 1990] have been reported. Whether or not there is sensitization or desensitization depends on the glucose concentration [Eizirik et al., 1992; Leahy et al., 1986; Sako and Grill, 1990] and the duration of glucose action [Bedoya and Jeanrenaud, 1991; Bolaffi et al., 1988]. Both, sensitization and desensitization, appear to be reversible on return to normal glucose or mild hypoglycemia [Leahy and Weir, 1991; Svenson and Hellerström, 1991]. It seems, however, that there is a fluent change from the first occurring hyperinsulinemia to hypoinsulinemia. In this lecture I first want to talk about the possible mechanism of sensitization of insulin secretion discussing previous results we have obtained from rat islets isolated after a 48 hours period of i.v. infusion with 50% glucose. In the second part I will discuss some of the findings coming from the respective literature concerning desensitization of insulin secretion.

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Section: Sensitization Of Insulin Secretionmentioning

confidence: 99%