Intramuscular glucagon as a provocative stimulus for the assessment of pituitary function: Growth hormone and cortisol responses

Rao, R. Govinda; Spathis, G.S.

doi:10.1016/0026-0495(87)90150-8

Cited by 90 publications

(84 citation statements)

References 21 publications

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“…Our Endocrine Unit uses the GST as the first-line GH provocation test (16), which has been validated previously (25,26) and has been shown to be equivalent to the ITT (27,28). The Endocrine Society in its recent guidelines acknowledged the role of the GST for the diagnosis of GHD, particularly in the face of the recent shortage of GHRH (29) and in cases where the ITT may be contra-indicated (9, 10).…”

Section: Discussionmentioning

confidence: 99%

Low prevalence of hypopituitarism after subarachnoid haemorrhage using confirmatory testing and with BMI-specific GH cut-off levels

Gardner

Javadpour

Stoneley

et al. 2013

European Journal of Endocrinology

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Objective: Hypopituitarism following subarachnoid haemorrhage (SAH) has been reported to be a frequent occurrence. However, there is considerable heterogeneity between studies with differing patient populations and treatment modalities and most importantly employing differing endocrine protocols and (normal) reference ranges of GH. We aimed to examine prospectively a cohort of SAH survivors for development of hypopituitarism post-SAH using rigorous endocrine testing and compare GH response to glucagon stimulation with a cohort of healthy controls of a similar BMI. Design and methods: Sixty-four patients were investigated for evidence of hypopituitarism 3 months post-SAH with 50 patients tested again at 12 months. Glucagon stimulation testing (GST), with confirmation of deficiencies by GHRH/arginine testing for GH deficiency (GHD) and short synacthen testing for ACTH deficiency, was used. Basal testing of other hormonal axes was undertaken. Results: Mean age of patients was 53G11.7 years and mean BMI was 27.5G5.7 kg/m 2 . After confirmatory testing, the prevalence of hypopituitarism was 12% (GHD 10%, asymptomatic hypocortisolaemia 2%). There was no association between hypopituitarism and post-SAH vasospasm, presence of cerebral infarction, Fisher grade, or clinical grading at presentation. There was a significant correlation between BMI and peak GH to glucagon stimulation in both patients and controls. Conclusions: Identification of 'true' GHD after SAH requires confirmatory testing with an alternative stimulation test and application of BMI-specific cut-offs. Using such stringent criteria, we found a prevalence of hypopituitarism of 12% in our population.

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Section: Discussionmentioning

confidence: 99%

Low prevalence of hypopituitarism after subarachnoid haemorrhage using confirmatory testing and with BMI-specific GH cut-off levels

Gardner

Javadpour

Stoneley

et al. 2013

European Journal of Endocrinology

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“…2b), consistent with the assumption that low corticosterone levels detected in those groups, promote increased glucagon secretion by pancreatic a-cells, as an homeostatic response to normalize plasma glucose concentration. High glucagon concentrations may also contribute to the marked increase in plasma ACTH levels found in adrenalectomized and autotransplanted rats (Table 1), since previous studies demonstrated that administration of glucagon evokes a considerably rise in the blood levels of ACTH [24,25]. It has also been reported that systemic or intracerebroventricular administration of glucagon raises plasma concentration of corticosterone in rats [26] and cortisol in humans [27,28].…”

Section: Discussionmentioning

confidence: 94%

The Role of Corticosterone in the Metabolic Recovery after Intrasplenic Adrenal Autotransplantation in Rats

2004

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Abstract. Transplantation of adrenal cortical tissue may represent an alternative treatment to reestablish glucocorticoid secretion in adrenal insufficiency. In the present work, performed in adrenalectomized rats and adrenalectomized rats with a complete autotransplanted adrenal into the spleen, several hormones and biochemical parameters were measured and compared to control animals, in order to examine hormone interactions. Rats were sacrificed three weeks after surgery, and plasma and tissue samples were obtained for hormone and biochemical measurements. In adrenalectomized animals, plasma corticosterone, aldosterone and insulin levels were profoundly decreased, whereas in autotransplanted rats plasma corticosterone levels showed a partial recovery, aldosterone plasma concentrations remained low, and plasma insulin levels increased to values close to those of the controls. Both groups showed a marked elevation of plasma ACTH levels, as well as significantly increased plasma glucagon concentrations. In autotransplanted animals, most of the biochemical parameters, which were altered in adrenalectomized rats, returned to normal levels. These results suggest that increased glucagon levels in adrenalectomized and autotransplanted animals, may contribute to the marked increase of plasma ACTH, and could also be important in the recovery of plasma glucose and hepatic glycogen observed in autografted rats. Since high glucagon concentrations alone were unable to normalize carbohydrate levels in adrenalectomized animals, it appears that glucagon can act only in the presence of corticosterone.

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“…glucagon administration is followed by a clear increase in ACTH and cortisol secretion (4,5). In fact, testing with glucagon is considered a reliable alternative to insulin-induced hypoglycemia for the diagnosis of secondary adrenal insuf®ciency (4,5,7).…”

Section: Discussionmentioning

confidence: 99%

“…In fact, glucagon is considered a classical provocative stimulus of GH secretion for the diagnosis of GH de®ciency (2±5, 8) and has been proposed by some authors as an alternative to insulin-induced hypoglycemia for the diagnosis of secondary adrenal insuf®ciency (4,5,7).…”

Section: Introductionmentioning

confidence: 99%

Interaction between glucagon and human corticotropin-releasing hormone or vasopressin on ACTH and cortisol secretion in humans

Arvat

Maccagno

Ramunni

et al. 2000

European Journal of Endocrinology

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Objective: It is known that glucagon administration elicits ACTH and cortisol responses in humans, although this effect takes place after intramuscular or subcutaneous but not after the intravenous route of administration. The mechanisms underlying this stimulatory effect on corticotroph secretion are unknown but they are unrelated to glucose variations and stress-mediated actions. Design and Methods: To throw further light on the stimulatory effect of i.m. glucagon on the pituitary± adrenal axis, using six normal young female volunteers (26±32 years, body mass index 19.7±22.5 kg/m 2 ) we studied the interaction between glucagon (GLU; 0.017 mg/kg i.m.) and human corticotropinreleasing hormone (hCRH; 2.0 mg/kg i.v.) or vasopressin (AVP; 0.17 U/kg i.m.). The interactions between hCRH and AVP on the hypothalamo±pituitary±adrenal (HPA) axis and the GH response to GLU alone or combined with hCRH or AVP were also studied. Results: GLU i.m. administration elicited a clear increase in ACTH (peak vs baseline, means 6 S.E.M.: 11.6 6 3.3 vs 4.2 6 0.3 pmol/l, P < 0.05), cortisol (613.5 6 65.6 vs 436.9 6 19.3 nmol/l, P < 0.05) and GH levels (11.6 6 3.4 vs 3.3 6 0.7 mg/l, P < 0.05). The ACTH response to GLU (area under the curve: 426.4 6 80.9 pmol/l per 120 min) was higher than that to AVP (206.3 6 38.8 pmol/l per 120 min, P < 0.02) and that to hCRH (299.8 6 39.8 pmol/l per 120 min) although this latter difference did not attain statistical signi®cance. The GLU-induced cortisol response (28 336.9 6 2430.7 nmol/l per 120 min) was similar to those after hCRH (24 099.2 6 2075.2 nmol/l per 120 min) and AVP (21 808.7 6 1948.2 nmol/l per 120 min). GLU and hCRH had an additive effect on ACTH (964.9 6 106.6 pmol/l per 120 min, P < 0.02) and a less than additive effect on cortisol levels (35 542.5 6 2720.2 nmol/l per 120 min). Similarly, GLU and AVP had an additive effect on ACTH (825.6 6 139.6 pmol/l per 120 min, P < 0.02) and an effect less than additive on cortisol levels (33 059.2 6 1965.3 nmol/l per 120 min). The effects of GLU co-administered with hCRH or AVP were similar to those of the combined administration of hCRH and AVP on ACTH (906.0 6 152.7 pmol/l per 120 min) and cortisol (34 383.5 6 1669.2 nmol/l per 120 min) levels. The GH response to GLU was not modi®ed by hCRH or AVP. Conclusions: These results show that i.m. glucagon administration is a provocative stimulus of ACTH and cortisol secretion, at least as potent as hCRH and AVP. The ACTH-releasing effect of i.m. glucagon is not mediated by selective CRH or AVP stimulation but the possibility that both neurohormones play a role could be hypothesized. European Journal of Endocrinology 143 99±104

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Intramuscular glucagon as a provocative stimulus for the assessment of pituitary function: Growth hormone and cortisol responses

Cited by 90 publications

References 21 publications

Low prevalence of hypopituitarism after subarachnoid haemorrhage using confirmatory testing and with BMI-specific GH cut-off levels

Low prevalence of hypopituitarism after subarachnoid haemorrhage using confirmatory testing and with BMI-specific GH cut-off levels

The Role of Corticosterone in the Metabolic Recovery after Intrasplenic Adrenal Autotransplantation in Rats

Interaction between glucagon and human corticotropin-releasing hormone or vasopressin on ACTH and cortisol secretion in humans

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