Effect of Insulin Induced Hypoglycaemia on the Blood Levels of Catecholamines, Glucagon, Growth Hormone, Cortisol, C-Peptide and Proinsulin Before and During Medication With the Cardioselective Beta-Receptor Blocking Agent Metoprolol in Man

Hökfelt, Bernt; Hansson, Bengt‐Göran; Hedïng, Lise G.; Nilsson, K. O.

doi:10.1530/acta.0.0870659

Cited by 23 publications

(9 citation statements)

References 20 publications

(21 reference statements)

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“…This effect was not due to a more pronounced hypoglvcaemia during betablockade since similar blood glucose levels were reached at nadir ( Table 2). The observation that metoprolol further elevates the adrenaline levels during hypoglvcaemia is in agreement with the Study of Hökfelt et al (1978) in non-diabetic hy¬ pertensives. However, our finding that also a nonselective beta-blocker, such as propranolol, leads to the same effect is at variance with these investi¬ gators studying penbutolol (Hansson & Hökfelt 1976).…”

Section: Discussionsupporting

confidence: 90%

“…The smaller rise in noradrenaline as compared to adrenaline during hypoglycaemia has also been found previously (Garber et al 1976;Hökfelt et al 1978) and is probably due to increased peripheral uptake and degradation.…”

Section: Discussionsupporting

confidence: 82%

“…The adrenaline levels reached during hypoglv¬ caemia without beta-blockers were less than those reported in non-diabetics in some studies (Christensen 1974;Garber et al 1976) but similar to another (Hökfelt et al 1978). It is, however, dif¬ ficult to make such comparisons since the catecholamine levels increase exponentially the lower the blood glucose levels (Christensen 1974) (Fig.…”

Section: Discussionsupporting

confidence: 59%

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Effect of beta-blockade on hormone release during hypoglycaemia in insulin-dependent diabetics

Lager¹,

Jagenburg²,

Schenck³

et al. 1980

Acta Endocrinologica

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Previous studies have shown that non-selective, but not beta1-selective, beta-blockers prolong the duration of hypoglycaemia. In order to elucidate possible mechanisms key hormones as well as alanine levels were measured following insulin-induced hypoglycaemia in 7 insulin-dependent diabetics. The subjects were treated with placebo, propranolol (a non-selective agent) or metoprolol (a beta1-selective drug) prior to the hypoglycaemia. Treatment with either beta-blocking agent led to higher levels of adrenaline, glucagon, cortisol and growth hormone during hypoglycaemia as compared to those reached on placebo. The adrenaline levels during placebo treatment in response to hypoglycaemia appeared less in these diabetics than that previously reported for non-diabetics. The plasma alanine levels were similar and decreased following insulin administration irrespective of type of treatment.The data show that the release of key glycogenolytic and gluconeogenic hormones is not inhibited by beta-blockers during hypoglycaemia but is instead augmented or, possibly, hormonal clearance is reduced. It is suggested that the delayed recovery in blood glucose on a non-selective beta-blocker is partly due to lack of gluconeogenic substrates such as lactate and glycerol.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 82%

Section: Discussionsupporting

confidence: 59%

See 1 more Smart Citation

Effect of beta-blockade on hormone release during hypoglycaemia in insulin-dependent diabetics

Lager¹,

Jagenburg²,

Schenck³

et al. 1980

Acta Endocrinologica

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“…Although circulating epinephrine and norepinephrine levels observed during hypoglycemia were increased by this maneuver, infusion of these agents had no effects on glucose counterregulation. Similar results have been obtained with measurements of circulating glucose levels (15,16) and glucose fluxes (17) in previous studies during selective a-or p-adrenergic blockade. These observations and those indicating that normal glucose recovery from insulin-induced hypoglycemia can occur in spinal cord transected (10,11) and in adrenalectomized (11)(12)(13)(14) Finally, it should be pointed out that in these latter studies some glucose counterregulation was evident despite apparent adrenergic blockade and inhibition of both glucagon and growth hormone secretion; plasma glucose and glucose appearance increased respectively from nadirs of 36+2 mg/dl and 0.88+0.08 mg/kg per min to peak values of 52+5 mg/dl and 2.02 +0.27 mg/kg per min.…”

Section: Discussionsupporting

confidence: 90%

“…However, factors other than catecholamines must be capable of restoring normoglycemiiia because apparently normal glucose counterregulation has been observed in catecholamine-deficient patients with spinal cord transections (10,11), epinephrine-deficient adrenalectomized patients (11)(12)(13)(14), and normal subjects during the infusioIn of a-or ,-adrenergic blocking agents (15)(16)(17).…”

Section: Introductionmentioning

confidence: 99%

Role of Glucagon, Catecholamines, and Growth Hormone in Human Glucose Counterregulation

1979

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A B S T R A C T To further characterize mechanisms of glucose counterregulation in man, the effects of pharmacologically inducd deficiencies of glucagon, growth hormone, and catecholamines (alone and in combination) on recovery of plasma glucose from insulin-induced hypoglycemia and attendant changes in isotopically ([3-3H]glucose) determined glucose fluxes were studied in 13 normal subjects. In control studies, recovery of plasma glucose from hypoglycemia was primarily due to a compensatory increase in glucose production; the temporal relationship of glucagon, epinephrine, cortisol, and growth hormone responses with the compensatory increase in glucose appearance was compatible with potential participation ofall these hormones in acute glucose counterregulation. Infusion of somatostatin (combined deficiency of glucagon and growth hormone) accentuated insulin-induced hypoglycemia (plasma glucose nadir: 36±2 ng/dl during infusion ofsomatostatin vs. 47±2 mg/dl in control studies, P < 0.01) and impaired restoration of normoglycemia (plasma glucose at min 90: 73±3 mg/dl at end ofsomatostatin infusion vs. 92±3 mg/dl in control studies, P < 0.01). This impaired recovery of plasma glucose was due to blunting of the compensatory increase in glucose appearance since glucose disappearance was not augmented, and was attributable to suppression of 62 glucagon secretion rather than growth hormone secretion since these effects of somatostatin were not observed during simultaneous infusion of somatostatin and glucagon whereas infusion of growth hormone along with somatostatin did not prevent the effects of somatostatin. The attenuated recovery of plasma glucose from hypoglycemia observed during somatostatininduced glucagon deficiency was associated with plasma epinephrine levels twice those observed in control studies. Infusion of phentolamine plus propranolol (combined a-and,8-adrenergic blockade) had no effect on plasma glucose or glucose fluxes after insulin administration. However, infusion of somatostatin along with both phentolamine and propranolol further impaired recovery ofplasma glucose from hypoglycemia compared to that observed with somatostatin alone (plasma glucose at end of infusions: 52+6 mg/dl for somatostatin-phentolamine-propranolol vs. 72+±5 mg/dl for somatostatin alone, P < 0.01); this was due to further suppression of the compensatory increase in glucose appearance (maximal values: 1.93±0.41 mg/kg per min for somatostatin-phentolamine-propranolol vs. 2.86+0.32 mg/kg per min for somatostatin alone, P < 0.05). These results indicate that in man (a) restoration of normoglycemia after insulin-induced hypoglycemia is primarily due to a compensatory increase in glucose production; (b) intact glucagon secretion, but not growth hormone secretion, is necessary for normal glucose counterregulation, and (c) adrenergic mechanisms do not normally play an essential role in this process but become critical to recovery from hypoglycemia when glucagon secretion is impaired.J. Clin. Invest.

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β‐Endorphin, ACTH, and catecholamine responses in chronic autonomic failure

Polinsky¹,

Brown²,

Lee³

et al. 1987

Annals of Neurology

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Plasma epinephrine (EPI), norepinephrine (NE), beta-endorphin, and corticotropin (ACTH) responses were measured during insulin-induced hypoglycemia in normal subjects and in patients with either multiple system atrophy (MSA) or idiopathic orthostatic hypotension (IOH). In normal subjects, there was a striking rise in EPI, NE, beta-endorphin, and ACTH following the nadir of hypoglycemia. Both beta-endorphin and ACTH responses were significantly lower than normal in patients with MSA, in contrast to normal levels in IOH patients. No correlation was observed between the degree of adrenergic insufficiency and the beta-endorphin and ACTH responses. The normal peptide responses in IOH are consistent with involvement limited to the peripheral sympathetic nervous system, whereas lesions in the central nervous system in MSA interfere with release of beta-endorphin and ACTH in response to hypoglycemia. The strong correlation between beta-endorphin and ACTH levels is consistent with their common origin. Peripheral adrenergic activity is not essential for beta-endorphin and ACTH release in humans.

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Effect of Insulin Induced Hypoglycaemia on the Blood Levels of Catecholamines, Glucagon, Growth Hormone, Cortisol, C-Peptide and Proinsulin Before and During Medication With the Cardioselective Beta-Receptor Blocking Agent Metoprolol in Man

Cited by 23 publications

References 20 publications

Effect of beta-blockade on hormone release during hypoglycaemia in insulin-dependent diabetics

Effect of beta-blockade on hormone release during hypoglycaemia in insulin-dependent diabetics

Role of Glucagon, Catecholamines, and Growth Hormone in Human Glucose Counterregulation

β‐Endorphin, ACTH, and catecholamine responses in chronic autonomic failure

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