Central α-Adrenergic Regulation of Growth Hormone and Insulin

Toivola, P. T. K.; Gale, C; Goodner, CJ; Werrbach, Jon H.

doi:10.1159/000178270

Cited by 51 publications

(9 citation statements)

References 36 publications

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“…kg -t-min -1, may stimulate a central/%adrenergic pathway capable of mediating increased insulin secretion. Toivola et al [13] found that the a-adrenergic blocking drug, phentolamine, elevates peripheral insulin levels when placed in the hypothalamus of baboons. Furthermore, several authors have drawn attention to the modulation of insulin secretion by the hypothalamus.…”

Section: Discussionmentioning

confidence: 99%

Differences between the effects of adrenaline and noradrenaline on insulin secretion in the dog

Ribes¹,

Blayac²,

Loubatières-Mariani³

1983

Diabetologia

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The effects of adrenaline and noradrenaline infusions on pancreaticoduodenal venous insulin output were studied in anaesthetized normal dogs. Two experimental protocols were used. In the first, the dogs had a normal blood glucose level at the start of the catecholamine infusion (normoglycaemic dogs). In the second, the animals were made hyperglycaemic by a continuous glucose infusion (hyperglycaemic dogs). In the normoglycaemic dogs, adrenaline (0.5 micrograms X kg-1 X min-1) provoked hyperglycaemia accompanied by an increase in insulin output. Noradrenaline (0.5 micrograms X kg-1 X min-1) also caused an increase in insulin output but without any significant change in blood glucose. In hyperglycaemic dogs, adrenaline (2 micrograms X kg-1 X min-1) reduced the insulin response and enhanced the hyperglycaemia; noradrenaline (2 micrograms X kg-1 X min-1) markedly increased the insulin response (+ 2250%) without any significant change in blood glucose. Propranolol (0.3 mg/kg, IV) prevented the increase of insulin induced by noradrenaline. These findings show that, in the normal dog, adrenaline and noradrenaline infusions can produce opposite effects on insulin response depending on the experimental conditions.

show abstract

Section: Discussionmentioning

confidence: 99%

Differences between the effects of adrenaline and noradrenaline on insulin secretion in the dog

Ribes¹,

Blayac²,

Loubatières-Mariani³

1983

Diabetologia

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“…Beyond these direct effects of adrenergic secretion, adrenergic recruitment, and coordination of glucagon, cortisol and growth hormone secretion may serve as an important reinforcement to other mechanisms increasing the secretion of these hormones, thereby augmenting the overall glycemic response. Growth hormone (71)(72)(73) and cortisol by way of ACTH secretion (72,74) are both increased by adrenergic hypothalamic mechanisms. Glucagon secretion can also be increased by adrenergic activity (75)(76)(77)(78).…”

Section: Discussionmentioning

confidence: 99%

The role of adrenergic mechanisms in the substrate and hormonal response to insulin-induced hypoglycemia in man.

Garber¹,

Cryer²,

Santiago³

et al. 1976

J. Clin. Invest.

362

135

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A B S T R A C T Sequential determinations of glucose outflow and inflow, and rates of gluconeogenesis from alanine, before, during and after insulin-induced hypoglycemia were obtained in relation to alterations in circulating epinephrine, norepinephrine, glucagon, cortisol, and growth hormone in six normal subjects. Insulin decreased the mean (+SEM) plasma glucose from 89+3 to 39+2 mg/dl 25 min after injection, but this decline ceased despite serum insulin levels of 153±22 gtU/ml.Before insulin, glucose inflow and outflow were constant, averaging 125.3±7.1 mg/kg per h. 15 min after insulin, mean glucose outflow increased threefold, but then decreased at 25 min, reaching a rate 15% less than the preinsulin rate. Glucose inflow decreased 80% 15 min after insulin, but increased at 25 min, reaching a maximum of twice the basal rate. Gluconeogenesis from alanine decreased 68% 15 min after insulin, but returned to preinsulin rates at 25 min, and remained constant for the next 25 min, after which it increased linearly. A fourfold increase in mean plasma epinephrine was found 20 min after insulin, with maximal levels 50 times basal. Plasma norepinephrine concentrations first increased significantly at 25 min after insulin, whereas significantly increased levels of cortisol and glucagon occurred at 30 min, and growth hormone at 40 min after insulin.Thus, insulin-induced hypoglycemia in man results from both a decrease in glucose production and an increase in glucose utilization. Accelerated glycogenolysis

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“…Thus, it has been demonstrated that perfusion of the hypothalamus in baboons with the alfa-adrenergic blocking agent, phentolamine, induced an enhancement of basal insulin secretion when administered in a concentration which had no effect when given to the systematic circulation [7]. Furthermore, lesions applied to the ventromedial nuclei of the hypothalamus were accompanied by hyperinsulinemia [8].…”

Section: Discussionmentioning

confidence: 99%

Effect of somatostatin on glucose induced insulin release in isolated perfused rat pancreas and isolated rat pancreatic islets

1974

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Central α-Adrenergic Regulation of Growth Hormone and Insulin

Cited by 51 publications

References 36 publications

Differences between the effects of adrenaline and noradrenaline on insulin secretion in the dog

Differences between the effects of adrenaline and noradrenaline on insulin secretion in the dog

The role of adrenergic mechanisms in the substrate and hormonal response to insulin-induced hypoglycemia in man.

Effect of somatostatin on glucose induced insulin release in isolated perfused rat pancreas and isolated rat pancreatic islets

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