Insulin binding and action in antibody-induced diabetes in the rat

Kemmler, Wolfgang; Häring, Hans‐Ulrich

doi:10.1007/bf00254302

Cited by 7 publications

(2 citation statements)

References 15 publications

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“…In the present paper we report a specific inhibition of insulin stimulation of D-glucose transport and a reduction in insulin binding at insulin con-Diabetes Association (Haring et al, 1982b) and the 1982 EASD meeting in Budapest (Kemmler et al, 1982).…”

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Catecholamine-induced insulin resistance of glucose transport in isolated rat adipocytes

Kirsch¹,

Baumgarten²,

Deufel³

et al. 1983

Biochemical Journal

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The effects of pre-incubation with isoprenaline and noradrenaline on insulin binding and insulin stimulation of D-glucose transport in isolated rat adipocytes are reported. (1) Pre-incubation of the cells with isoprenaline (0.1-10 microM) in Krebs-Ringer-Hepes [4-(2-hydroxyethyl)-1-piperazine-ethanesulphonic acid] buffer (30 min, 37 degrees C) at D-glucose concentrations of 16 mM, in which normal ATP levels were maintained, caused a rightward-shift in sensitivity of D-glucose transport to insulin stimulation by 50% and a decrease in maximal responsiveness by 30% (2) [A14-125I]insulin binding was reduced significantly by 35% at insulin concentrations less than 100 mu-units/ml and Scatchard analysis showed that this consisted mainly of a decrease in high-affinity binding. (3) Pre-incubation with catecholamines under the same conditions but at low glucose concentrations (0-5 mM) caused a fall in intracellular ATP levels of 65 and 45% respectively. (4) The fall in ATP additionally lowered insulin binding by 50% at all insulin concentrations and a parallel shift of the binding curves in the Scatchard plot showed that this was due to a decrease in the number of receptors. (5) At low and high ATP concentrations the insulin stimulation of D-glucose transport was inhibited to a similar extent. (6) Pre-incubation with catecholamines thus inhibited insulin stimulation of D-glucose transport in rat adipocytes mainly by a decrease in high-affinity binding of insulin, which was not mediated by low ATP levels. This mechanism may play a role in the pathogenesis of catecholamine-induced insulin resistance in vivo.

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supporting

confidence: 50%

Catecholamine-induced insulin resistance of glucose transport in isolated rat adipocytes

Kirsch¹,

Baumgarten²,

Deufel³

et al. 1983

Biochemical Journal

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“…(2) The effect observed in vivo might be secondary to changes in the insulin serum levels during the sulphonylurea therapy. It is well established that the insulin receptor capacity is inversely related to the insulin plasma levels in the state of insulin deficiency [22,23]. Decreasing insulin levels during sulphonylurea therapy were observed earlier by different investigators [19,20] and also recently by Lunetta et al [21] and by Beck-Nielsen et al [18] with adult-onset diabetic patients.…”

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confidence: 81%

Extrapancreatic action of the sulphonylurea gliquidone: post-receptor effect on insulin-stimulated glycogen synthesis in rat hepatocytes in primary culture

et al. 1984

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Summary. The effects of a sulphonylurea, gliquidone, on insulin binding and the insulin induced rate of glycogen synthesis, were studied in rat hepatocytes in primary culture. Hepatocytes were cultured for 48 h. During the second 24 h of this period, the hepatocytes were incubated with or without gliquidone (5 mg/1). The binding of 125I-insulin and the insulin stimulation of glycogen synthesis from aac-glucose were measured. Gliquidone influenced neither insulin binding nor the basal rate of glycogen synthesis, but it did enhance the effect of insulin on glycogen synthesis. Responsiveness was increased by gliquidone at all insulin concentrations used (10-10,000 mU/1); at 1000 mU/1 the drug increased glycogen synthesis from 310 to 430% above the basal rate. Half-maximal stimulation was reached in control cells at an insulin concentration of 95 mU/l and in gliquidone-treated cells at 94 mU/1, which indicates unchanged insulin sensitivity. Based on these experiments with cultured rat hepatocytes it appears that the extrapancreatic action of gliquidone is not mediated by an effect on insulin binding.

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Cyclic AMP modulates insulin binding and induces post-receptor insulin resistance of glucose transport in isolated rat adipocytes

Kirsch

Kemmler

Häring

1983

Biochemical and Biophysical Research Communications

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Insulin binding and action in antibody-induced diabetes in the rat

Cited by 7 publications

References 15 publications

Catecholamine-induced insulin resistance of glucose transport in isolated rat adipocytes

Catecholamine-induced insulin resistance of glucose transport in isolated rat adipocytes

Extrapancreatic action of the sulphonylurea gliquidone: post-receptor effect on insulin-stimulated glycogen synthesis in rat hepatocytes in primary culture

Cyclic AMP modulates insulin binding and induces post-receptor insulin resistance of glucose transport in isolated rat adipocytes

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