Counterregulatory hormone release after human and porcine insulin in healthy subjects and patients with pituitary disorders

Landgraf-Leurs, M. M. C.; Brügelmann, I.; Kämmerer, Susanne; Lorenz, Rodney A.; Landgraf, R.

doi:10.1007/bf01716462

Cited by 20 publications

(10 citation statements)

References 27 publications

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“…Our results of oCRF and hCRF stimula tion of ACTH and cortisol secretion show a significant lower increase of these hormones in comparison to insulin-induced hypoglyce mia test in normal volunteers [6]. This obser vation may be explained by the findings of Rivieret al [14] in rats and by Liu et al [7] in humans who showed a higher response after the combined administration of CRF and arginine vasopressin than after the adminis tration of CRF or arginine vasopressin alone.…”

Section: Crf Stimulation In Normalssupporting

confidence: 32%

Corticotropin-Releasing Factor in Humans

Stalla¹,

Stalla²,

Schopohl³

et al. 1986

Horm Res

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The biological activity of ovine (o) and human (h) corticotropin-releasing factor (CRF) in normal volunteers was investigated, using bolus injections with different CRF dosages. There was a significant increase of ACTH, β-endorphine and cortisol after the injection of all dosages. Repetitive stimulation and continuous infusion of hCRF lead to repetitive release of identical amounts of ACTH or constant elevation of ACTH levels. oCRF and hCRF serum immunoreactivity was measured with specific radioimmunoassays after bolus injection, pulsatile administration and infusion of CRF. The half-time of serum disappearance after acute injection studies was calculated as 9 min for hCRF dand 18 min for oCRF. The ‘metabolic clearance’ of hCRF calculated using the infusion study was 2.72 ml/min × kg. Endogenous CRF immunoreactivity was detectable in 14 patients during insulin hypoglycemia and in 86 out of 97 pregnant females. Furthermore, CRF could be extracted from human placenta. The chromatographic pattern of extracted placenta CRF, pregnancy serum CRF and CRF standard preparation was identical. Furthermore, CRF immunoreactivity was detectable in some patients with different causes of ACTH hypersecretion.

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Section: Crf Stimulation In Normalssupporting

confidence: 32%

Corticotropin-Releasing Factor in Humans

Stalla¹,

Stalla²,

Schopohl³

et al. 1986

Horm Res

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“…In contrast, peak and integrated prolactin responses to the biopotent-equivalent dose of proinsulin were reduced compared with responses to insulin, which implies that either proinsulin-induced hypoglycemia is a submaximal stimulus for prolactin secretion or the peptide exhibits inhibitory effects on prolactin secretion at the hypothalamic or pituitary level. Previous studies have demonstrated that prolactin responses to human insulin are reduced compared with responses to pork insulin, despite identical hypoglycemia (3,11). This finding suggests that the administered peptide may be an important determinant of prolactin responses and provides supportive evidence for the latter possibility.…”

Section: Methodsmentioning

confidence: 76%

Differential Effects of Insulin- and Proinsulin-Induced Hypoglycemia on Pituitary Hormone and Catecholamine Secretion

Williams¹,

Berelowitz

Berk

et al. 1987

Diabetes Care

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The effects of insulin- and proinsulin-induced hypoglycemia on pituitary hormone and catecholamine secretion were compared in normal men to search for possible hypothalamic or pituitary inhibitory effects of proinsulin on glucocounterregulatory responses. When subjects received 0.1 U/kg i.v. human insulin and 25-38 micrograms/kg i.v. human proinsulin on separate occasions, plasma glucose decreased more rapidly after insulin, and the nadir was slightly lower, but integrated hypoglycemic responses were similar. Cortisol, growth hormone (GH), prolactin, epinephrine, and norepinephrine responses occurred more rapidly after insulin than after proinsulin. Peak and integrated cortisol, GH, and catecholamine responses to insulin and proinsulin were similar, but those of prolactin were reduced after proinsulin when compared with insulin by 42% (P less than .01) and 34% (P less than .05), respectively. When euglycemia was maintained by a variable glucose infusion rate after the injection of insulin and proinsulin, no differences were observed in plasma levels of any of the hormones. The intravenous injection of a dose of proinsulin (6 micrograms/kg), which did not produce hypoglycemia but was the molar equivalent of insulin used in the first protocol, failed to modify the GH or prolactin responses to a combined injection of GH-releasing hormone (1 microgram/kg) and thyrotropin-releasing hormone (500 micrograms). Our results indicate that the onset of pituitary hormone and catecholamine responses to hypoglycemia are related to the rate of plasma glucose decline, with the slower responses to proinsulin reflecting a more gradual onset of hypoglycemia. The magnitude of the cortisol, GH, and catecholamine responses, however, was comparable with proinsulin- and insulin-induced hypoglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…IHT stimulates ACTH and GH secretion by activat ing hypothalamic centers [4,19]. In contrast, CRH and GRH lead to ACTH and GH secretion by activating the anterior pituitary directly.…”

Section: Discussionmentioning

confidence: 99%

“…Blood was taken directly before, 30, 45, 60 and 90 min after insulin administration. The test was regarded as adequate, if the blood sugar was lowered below 40 mg/dl [4], The IHT was not performed in those patients who had already unmeasurable basal cortisol levels.…”

Section: Insulin Hypoglycemia Testmentioning

confidence: 99%

“…Insulin hypoglycemia activates the whole hypothalamo-pituitary-adrenal axis [4,6] and stimulates growth hormone (GH) secretion at a hypothalamic level [4]. The recently discovered corticotropin-releasing hormone (CRH) and growth hormone-releasing hormone (GRH) stimulate adrenocorticotropic hormone (ACTH) [2,11] and GH secretion at the pituitary level [24].…”

Section: Introductionmentioning

confidence: 99%

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Insulin Hypoglycemia Test and Releasing Hormone (Corticotropin-Releasing Hormone and Growth Hormone-Releasing Hormone) Stimulation in Patients with Pituitary Failure of Different Origin

et al. 1988

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To investigate the efficacy of endocrine evaluation in diagnosing and localizing the cause of anterior pituitary failure, 17 patients with suprasellar space-occupying lesions, 4 patients with intrasellar tumors, 8 patients with no detectable anatomical lesion, 1 patient with posttraumatic failure and 1 patient with septooptical dysplasia were investigated. Endocrine evaluation consisted of measuring adrenocorticotropic hormone (ACTH), cortisol, and growth hormone (GH) levels during insulin hypoglycemia test (IHT) and after administration of corticotropin-releasing hormone (CRH) and growth hormone-releasing hormone (GRH). In addition, basal prolactin levels, gonadal and thyroid function were evaluated. The results showed that 4 of 17 patients with suprasellar tumors had normal ACTH and GH responses during IHT and after releasing hormone (RH) administration. Five of these patients had a normal ACTH or cortisol rise but no GH response during IHT. All 5 had a normal ACTH and 3 had normal GH rise after RH. Seven patients with suprasellar tumors had no ACTH or GH response during IHT, but all had an ACTH response to CRH. Only 3 of this group had a GH response to GRH. There was one exception of a patient who showed a GH and ACTH rise during IHT but only a blunted ACTH and no GH rise after RH administration. Four patients with pituitary failure and no demonstrable lesion had an ACTH rise after CRH but no GH rise after GRH, whereas in 3 patients with isolated ACTH deficiency no ACTH rise after CRH was seen. In 4 patients with nonsecreting pituitary tumors normal ACTH responses to IHT and CRH were seen, whereas GH rose during IHT only in 1 patient. Thirteen of all patients had elevated prolactin levels above 500 µU/ml. Eight of these patients had ACTH and GH secretion patterns compatible with a hypothalamic defect, i.e. no response during IHT but an ACTH or GH response or both after RH administration. However, 5 patients with a bonafide pituitary tumor and nonresponsiveness to the releasing hormone had also elevated prolactin levels. In 2 patients with moderate hyper-prolactinemia, ACTH and GH responses to IHT and RH were completely normal. Our findings show that the endocrine function tests used in this study are not always reliable in locating the hypothalamo-pituitary defect.

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Counterregulatory hormone release after human and porcine insulin in healthy subjects and patients with pituitary disorders

Cited by 20 publications

References 27 publications

Corticotropin-Releasing Factor in Humans

Corticotropin-Releasing Factor in Humans

Differential Effects of Insulin- and Proinsulin-Induced Hypoglycemia on Pituitary Hormone and Catecholamine Secretion

Insulin Hypoglycemia Test and Releasing Hormone (Corticotropin-Releasing Hormone and Growth Hormone-Releasing Hormone) Stimulation in Patients with Pituitary Failure of Different Origin

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