Significance of epinephrine in insulin hypoglycemia in man

Wallace, John M.; Harlan, William R.

doi:10.1016/0002-9343(65)90131-2

Cited by 31 publications

(10 citation statements)

References 19 publications

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“…The suggestion of several groups of investigators (Christensen et al 1975;De Fronzo et al 1977;Wallace & Harlan 1965;Di Salvo et al 1956) that the degree of hypoglycaemia quantitatively deter¬ mines the secretion of epinephrine is not fully supported by our findings. Our normal subjects showed marked individual differences with regard to the maximal epinephrine secretion.…”

Section: Discussioncontrasting

confidence: 84%

Insulin hypoglycaemia in normal and adrenalectomized subjects: comparison of metabolic parameters and endocrine counter regulation

Altorfer¹,

Ziegler²,

Froesch³

1981

Acta Endocrinologica

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Insulin tolerance tests were carried out in normal subjects and in adrenalectomized (ADX) patients in order to better understand the importance of counter regulatory hormones for the recovery from hypoglycaemia.Compared to normal subjects recovery of plasma glucose and of free fatty acid levels in adrenalectomized patients is retarded. The levels of glucagon are significantly higher in ADX patients during rest than in normal subjects. As expected, epinephrine and norepinephrine levels did not increase in ADX patients and, accordingly, blood pressure did not change. Growth hormone levels were the same in both groups of subjects. Interestingly, there was no clear-cut difference with regard to subjective symptoms of hypoglycaemia. It would appear that epinephrine is important for the rapid initial recovery from hypoglycaemia, whereas other hormones play a more important role later on.

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Section: Discussioncontrasting

confidence: 84%

Insulin hypoglycaemia in normal and adrenalectomized subjects: comparison of metabolic parameters and endocrine counter regulation

Altorfer¹,

Ziegler²,

Froesch³

1981

Acta Endocrinologica

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“…This is in good agreement with previous reports [5,9], but it contradicts the findings o f others who reported that insulin administration triggers a biphasic response o f plasma Epi, i.e. either a sharp increase followed by a plateauing response [3,4] or a moderate increase followed by a sharp and linear increase in plasma Epi [33], However, in these latter studies, laboratory animals underwent anesthesia and surgery immediately before insulin administration.…”

Section: Ly 53857supporting

confidence: 88%

Influence of 5-HT<sub>1</sub> and 5-HT<sub>2</sub> Receptor Antagonists on Insulin-Induced Adrenomedullary Catecholamine Release

1991

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Previous works have indicated that insulin stress activates the serotonin (5-HT) and sympathoadrenal systems in the fasted rat. In addition, recent studies have shown that activation of either the 5-HT_1A, the 5-HT_1C or the 5-HT₂ receptor triggers adrenal catecholamine release. Then, the aim of this study was to investigate whether brain 5-HT, by means of these receptors, mediates insulin-induced adrenal catecholamine release. For that purpose, both plasma epinephrine (Epi), norepinephrine (NE) and glucose levels were measured in conscious rats bearing intracardiac catheters. The intravenous administration of insulin (1 IU/ kg) triggered hypoglycemia throughout the following 120 min in both fed and overnight fasted rats. Insulin stress elicited within 30 min a 5- and 38-fold increase in plasma Epi levels in fed and fasted rats, respectively. This change was associated with significant elevations in plasma NE levels in the fasted rats only. The intravenous administration of the mixed 5-HTIA receptor/β-adrenocep-tor blocker (–)-propranolol (5 mg/kg) to fasted rats did not modify plasma glucose and catecholamine peak responses to insulin; however, at later times, insulin triggered hypoglycemic convulsions in (–)-propranolol- but not in saline-pretreated rats. Besides, pretreatments with the 5-HT_1C5-HT₂ receptor blocker LY 53857 (0.5 mg/kg), or the 5-HT₁/5-HT₂ receptor antagonist metergoline (3 mg/kg), did not diminish plasma catecholamine responses to insulin stress. Similarly, none of these antagonists affected plasma glucose recovery. These results seem to indicate that the sympathoadrenal response to insulin administration is not mediated by 5-HT.

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“…Considerable experimental evidence has accumulated indicating that the integrity of the sympathoadrenal axis is necessary for the hyperglycemic response to acute glucopenia (1)(2)(3). However, the relative importance of adrenal medullary catecholamines in the counter-regulatory events during hypoglycemia in man has yet to be defined (4). Since spinal cord transection or adrenergic blockade in animals prevented hyperglycemia, fatty acid mobilization, and the catecholamine secretory response to glucopenia (5,6), it seemed appropriate to examine, in man, the effect of spinal cord transection and adrenergic insufficiency on the counterregulatory response to acute glucose deprivation.…”

Section: Introductionmentioning

confidence: 99%

Neural Control of Counter-Regulatory Events during Glucopenia in Man

Brodows¹,

Pi‐Sunyer²,

Campbell³

1973

J. Clin. Invest.

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A B S T R A C T The effect of autonomic denervation on the metabolic and hormonal responses during intracellular glucopenia in man was investigated. 2-Deoxy-dglucose (2 DG), a competitive inhibitor of glucose metabolism, was administered intravenously to nine normal volunteers and to five patients, three with complete cervical cord transection (C-6) and two with idiopathic orthostatic hypotension. Before, during, and after a 20 min infusion of 2 DG (50 mg/kg) plasma concentrations of glucose, lactate, FFA, total catecholamines, immunoreactive insulin (IRI), human growth hormone (HGH), and cortisol were determined for periods up to 150 min. In control subjects, the initial elevation of FFA, glucose, HGH, and cortisol corresponded with the rise in total catecholamines, with maximal levels attained at 60 min, lactate rose at a slower rate, reaching peak levels at 150 min; although no change in IRI was noted. In contrast, 2 DG-induced glucopenic stress in the autonomic denervated subjects was characterized by no detectable catecholamine release or significant rise in glucose, FFA, lactate, or IRI. However, HGH and cortisol responses in four of the five patients were of a similar or greater magnitude than controls.These studies demonstrate that the integrity of the sympathoadrenomedullary axis is essential for the counter-regulatory response to intracellular glucopenia in man. Cortisol and HGH have no apparent role in these events.

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Significance of epinephrine in insulin hypoglycemia in man

Cited by 31 publications

References 19 publications

Insulin hypoglycaemia in normal and adrenalectomized subjects: comparison of metabolic parameters and endocrine counter regulation

Insulin hypoglycaemia in normal and adrenalectomized subjects: comparison of metabolic parameters and endocrine counter regulation

Influence of 5-HT<sub>1</sub> and 5-HT<sub>2</sub> Receptor Antagonists on Insulin-Induced Adrenomedullary Catecholamine Release

Neural Control of Counter-Regulatory Events during Glucopenia in Man

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