Direct Effect of Corticosterone upon Insulin Secretion Studied by Three Different Techniques

Billaudel, B.; Sutter, B. C. J.

doi:10.1055/s-0028-1092779

Cited by 72 publications

(39 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Qualitative and quantitative differences were however observed in the second secretory phase. The perfused rat pancreas presented a second phase of insulin secretion which increased progressively with high glucose concentrations, as also observed by others [10,11,12,13]. In the dormouse, a constant insulin flow in the late phase was rapidly reached.…”

Section: Comparison Of Insulin Secretion Of the Perfused Rat And Edibsupporting

confidence: 49%

Dynamics of insulin release by perfused edible dormouse (Glis glis) pancreas

Castex

1981

Diabetologia

View full text Add to dashboard Cite

Summary.In order to characterize seasonal variations of beta cell function in the edible dormouse (Glis glis), the dynamics of insulin release were examined during perfusion of the isolated pancreas. The B cells exhibited biphasic insulin secretion; however, the dynamic response differed from that of the rat in that there was a steady-state second release phase. Glucose-induced insulin release changed according to the seasons. With 16.8 mmol/1 glucose, the average insulin release of the late phase was 30.8 + 12.6 ng/min in winter, 7.4 + 3.2 ng/min in spring, 13.1 + 3 ng/min in summer and 23.3 + 4.4 ng/min in autumn. The glucose-induced insulin release, expressed as percent of the insulin content of the pancreas, varied according to the season: it represented 2.23 + 0.31% in winter, 1.28 + 0.10% in spring, 1.56 + 0.15 in summer and 2.6 + 0.11 in autumn. It is suggested that in spring and summer, the edible dormouse B cell secretion mechanism is less sensitive to glucose than in the other seasons.Key words: Edible dormouse (Glis glis), hibernating mammal, dynamics of insulin release, insulin secretion, glucose-stimulated insulin secretion, perfused pancreas, B cell, seasonal variations.Glucose tolerance tests performed in the edible dormouse have shown seasonal variations in the plasma insulin response, associated with glucose tolerance changes [1]. In autumn and in winter, the glucoseinduced plasma insulin concentrations are increased and insulin regulates the high peripheral consumption of this hexose; at the beginning of spring, it decreases and glucose tolerance is impaired. In June plasma insulin levels are low and poor glucose tolerance persists.Glucose tolerance tests give useful information about glucose effects on B cell function. In vivo tests are limited however, in that insulin secretagogues could act through secondary effects rather than through a direct action on the B cell [2]. In order to circumvent this problem and to discover if seasonal variations of plasma insulin levels after glucose loading are due to variations of insulin secretion, we have studied insulin secretion of the perfused pancreas of the edible dormouse and compared values with those found in the rat. Material and Methods

show abstract

Section: Comparison Of Insulin Secretion Of the Perfused Rat And Edibsupporting

confidence: 49%

Dynamics of insulin release by perfused edible dormouse (Glis glis) pancreas

Castex

1981

Diabetologia

View full text Add to dashboard Cite

show abstract

“…These results are difficult to interpret because of differing strains of animals and of doses and durations of administration of glucocorticoids. Glucocorticoids in vitro have also been reported to inhibit [34] or had no effect [36] on insulin release. In transgenic compared with control islets, glucose-induced insulin release was decreased and dexamethasone further decreased insulin release.…”

Section: Discussionmentioning

confidence: 99%

Increased glucocorticoid sensitivity in islet beta-cells: effects on glucose 6-phosphatase, glucose cycling and insulin release

et al. 1998

View full text Add to dashboard Cite

Glucose-6-phosphatase (G6Pase) and glucokinase activities can be demonstrated in pancreatic islets from mammalian species [1±4]. Glucokinase appears to be the rate limiting enzyme of glycolysis in the beta-cell, regulating the dose-response relationship between glucose utilization and insulin release [4]. Since G6Pase opposes the action of glucokinase, a possible role for G6Pase in the metabolic regulation of insulin release was postulated [2,3]. There are several reports of relatively low G6Pase activity in homogenates of normal mammalian islets [1±4], one of activity exceeding that in liver [5] and one of no activity [6]. We found low activity in permeabilized and sonicated islets from normal rats and mice [7]. Sweet et al. [8] also found low G6Pase activity in intact islets from normal rats.Glucose cycling is the simultaneous phosphorylation of glucose to glucose-6-P and dephosphorylation of glucose-6-P to glucose with the resulting consumption of ATP [9]. In accordance with reports of low G6Pase activity, we demonstrated a low rate of glucose cycling in intact islets from normal mice, dephosphorylation occurring at only 3 % of the rate of phosphorylation [10]. However, in islets from ob/ob mice, 30±40 % of phosphorylated glucose was dephosphorylated [10]. Glucose cycling was also increased in islets from other animal models of Type II diabetes [11,12]. In accordance with these results, G6Pase activity was several fold higher in islets from diabetic than normal animals [7,13] and islet G6Pase gene expression was increased during the development of diabetes in Zucker rats [14]. Diabetologia (1998) Summary Glucose-6-phosphatase (G6Pase) activity and the rate of glucose cycling are increased in islets from animal models of Type II (non-insulin-dependent) diabetes mellitus. Glucocorticoid treatment further stimulates these processes and inhibits glucose-induced insulin release. To determine whether these effects result from a direct action of glucocorticoids on the beta-cells, we used isolated islets. The islets were from transgenic mice overexpressing the glucocorticoid receptor in their beta-cells to increase the cells' sensitivity to glucocorticoid. Islets from transgenic and non-transgenic control mice utilized and oxidized the same amount of glucose. In contrast, islet G6Pase activity was 70 % higher, glucose cycling was increased threefold and insulin release was 30 % lower in islets from transgenic mice. Hepatic G6Pase activity was the same in transgenic and control mice. Dexamethasone administration increased G6Pase activity and glucose cycling and decreased insulin release in both transgenic and control mouse islets. We conclude that glucocorticoids stimulate islet G6Pase activity and glucose cycling by acting directly on the beta-cell. That activity may be linked to the inhibition of insulin release. [Diabetologia (1998) 41: 634±639]

show abstract

“…The direct in vitro effects of GCs on glucose-stimulated insulin secretion (GSIS) are generally inhibitory and occur within a few minutes, as demonstrated in isolated rat islets exposed to corticosterone (0.02-20 mg/l) (Billaudel & Sutter 1979;Fig. 2A, left).…”

Section: Acute Effects Of Gcsmentioning

confidence: 99%

Glucocorticoid treatment and endocrine pancreas function: implications for glucose homeostasis, insulin resistance and diabetes

Rafacho¹,

Ortsäter²,

Nadal³

et al. 2014

Journal of Endocrinology

177

114

View full text Add to dashboard Cite

Glucocorticoids (GCs) are broadly prescribed for numerous pathological conditions because of their anti-inflammatory, antiallergic and immunosuppressive effects, among other actions. Nevertheless, GCs can produce undesired diabetogenic side effects through interactions with the regulation of glucose homeostasis. Under conditions of excess and/or long-term treatment, GCs can induce peripheral insulin resistance (IR) by impairing insulin signalling, which results in reduced glucose disposal and augmented endogenous glucose production. In addition, GCs can promote abdominal obesity, elevate plasma fatty acids and triglycerides, and suppress osteocalcin synthesis in bone tissue. In response to GC-induced peripheral IR and in an attempt to maintain normoglycaemia, pancreatic b-cells undergo several morphofunctional adaptations that result in hyperinsulinaemia. Failure of b-cells to compensate for this situation favours glucose homeostasis disruption, which can result in hyperglycaemia, particularly in susceptible individuals. GC treatment does not only alter pancreatic b-cell function but also affect them by their actions that can lead to hyperglucagonaemia, further contributing to glucose homeostasis imbalance and hyperglycaemia. In addition, the release of other islet hormones, such as somatostatin, amylin and ghrelin, is also affected by GC administration. These undesired GC actions merit further consideration for the design of improved GC therapies without diabetogenic effects. In summary, in this review, we consider the implication of GC treatment on peripheral IR, islet function and glucose homeostasis.

show abstract

Direct Effect of Corticosterone upon Insulin Secretion Studied by Three Different Techniques

Cited by 72 publications

References 4 publications

Dynamics of insulin release by perfused edible dormouse (Glis glis) pancreas

Dynamics of insulin release by perfused edible dormouse (Glis glis) pancreas

Increased glucocorticoid sensitivity in islet beta-cells: effects on glucose 6-phosphatase, glucose cycling and insulin release

Glucocorticoid treatment and endocrine pancreas function: implications for glucose homeostasis, insulin resistance and diabetes

Contact Info

Product

Resources

About