bluuebunny/crossref_metadata_2025_split huggingface dataset:
ESCAPE FROM DEXAMETHASONE‐INDUCED ACTH AND CORTISOL SUPPRESSION BY CORTICOTROPHIN‐RELEASING HORMONE: MODULATORY EFFECT OF BASAL DEXAMETHASONE LEVELS
Authors: HERMUS A. R. M. M. , PIETERS G. F. F. M. , PESMAN G. J. , HOFMAN J. , SMALS A. G. H. , BENRAAD TH.J. , KLOPPENBORG P. W. C. 
Published: March 2008

SUMMARYThe response of ACTH and Cortisol to corticotrophin‐releasing hormone (CRH) after pretreatment with various doses of dexamethasone was investigated in five healthy subjects. The five subjects participated in six experiments. In each experiment 200 μg ovine CRH was administered as an i.v. bolus injection at 0900 h after pretreatment with respectively: (A) 1 mg dexamethasone orally at 2300 h in the evening before CRH injection, (B) 2 mg dexamethasone orally at 2300 h in the evening before CRH injection, (C) 4 mg dexamethasone orally at 2300 h in the evening before CRH injection, (D) 2 mg dexamethasone orally at 2300 h in the evening before CRH injection, followed by 2 mg dexamethasone orally 1 h before CRH, (E) no dexamethasone and (F) 1 mg dexamethasone orally 1 h before CRH injection. In spite of overnight suppression with a single dose of dexamethasone CRH elicited Cortisol rises in all individuals (experiments A‐C). Dexamethasone pretreatment in experiment D abolished the CRH‐induced stimulation of the pituitary‐adrenal axis. There was a significant and negative correlation between the basal dexamethasone levels (i.e. the dexamethasone levels immediately before CRH administration) in the experiments A‐D and the areas under the individual ACTH (R=−0.62; P < 0.01 by Spearman's rank correlation test) and Cortisol (R=−0.81; P < 0.001 by Spearman's test) curves, i.e. the lower the basal dexamethasone levels, the greater the rise in ACTH and Cortisol levels after CRH administration. Pretreatment with a single dose of 1 mg dexamethasone 1 h before CRH injection (experiment F) led to a significant inhibition of the CRH‐induced ACTH and Cortisol response, despite unsuppressed pre‐CRH ACTH and Cortisol levels. We conclude that CRH is able to overrule the inhibition of the pituitary‐adrenal axis by overnight suppression with pharmacological doses of dexamethasone. The strongly negative correlation between the basal dexamethasone levels and the CRH‐induced pituitary‐adrenal responses suggests that circulating glucocorticoid levels modulate the response of ACTH and Cortisol to CRH.
GROWTH HORMONE PRETREATMENT IN MAN BLOCKS THE RESPONSE TO GROWTH HORMONE‐RELEASING HORMONE; EVIDENCE FOR A DIRECT EFFECT OF GROWTH HORMONE
Authors: ROSS R. J. M. , BORGES F. , GROSSMAN A. , SMITH R. , NGAHFOONG L. , REES LESLEY H. , SAVAGE M. O. , BESSER G. M. 
Published: March 2008

SUMMARYThe effect of pretreatment with biosynthetic methionyl human GH (hGH) on the GH response to GHRH has been studied in normal subjects. Eight volunteers were given either 4IU hGH or placebo s.c. 12‐hourly for 72 h before a GHRH test, or a single s.c. dose of 4 IU hGH 12 h before a GHRH test. Somatomedin‐C (Sm‐C) levels at the time of the GHRH tests were significantly elevated after treatment with hGH compared to placebo, and the GH response to GHRH was significantly attenuated. A further six subjects were given 2 IU hGH or placebo i.v., and i.v. GHRH 3 h later; there was no rise in Sm‐C for the 5 h of the study after either treatment; nevertheless, the response to GHRH was completely abolished by pretreatment with hGH. These results demonstrate that GH can regulate its own secretion independently of changes in Sm‐C levels, through a mechanism other than the inhibition of GHRH release. The attenuated response to GHRH in the presence of elevated Sm‐C levels may be related to Sm‐C, or be a more direct effect of the recently elevated GH levels.
AN OPEN‐LABELLED STUDY OF THE SAFETY, ACUTE METABOLIC ACTIVITY AND PHARMACOKINETIC PROFILE OF A SHORT‐TERM COURSE OF RECOMBINANT HUMAN GROWTH HORMONE IN HEALTHY VOLUNTEERS
Authors: WILTON P. , SIETNIEKS ANNI 
Published: March 2008

SUMMARYThe safety and short‐term biological effects of recombinant human GH (Genotropin, KmbiVitrum AB, Stockholm, Sweden), given i.m. (8 IU/d) for 4 consecutive days to 10 healthy male volunteers, have been evaluated. No adverse reactions were detected by clinical investigation. Haematological parameters, clinical chemistry and the acute phase inflammatory profile showed no negative effects of the drug. The well‐known metabolic effects of GH were seen as an increase in free fatty acids and in the somatomedin level (IGF‐1). No antibodies to GH or periplasmic Escherichia coli peptides developed during the first month after treatment. The peak plasma level of hGH (62 ± 20 mU/1) occurred between 3.0 and 3.5 h. This study shows that recombinant hGH induces no toxic or other adverse reactions and that the acute metabolic effects and the pharmacokinetic profiles are comparable to those reported after injections of GH extracted from pituitary glands.
POSITIVE AND NEGATIVE FEED‐BACK EFFECT OF PROGESTERONE ON LUTEINIZING HORMONE SECRETION IN POST‐MENOPAUSAL WOMEN
Authors: STEELE P. A. , JUDD S. J. 
Published: March 2008

SUMMARYProgesterone is known to exert a biphasic feedback effect on luteinizing hormone (LH) secretion in animals and it has been demonstrated that this effect is dependent upon both duration of exposure to progesterone and the dose administered. In this paper we sought to determine whether a similar biphasic effect exists in humans. The pattern of LH secretion was assessed in six healthy oestrogen treated post‐menopausal women before and after they were given progesterone (50 mg/day) for 1 and 7 days. Progesterone treatment for 1 day resulted in a significant elevation in the basal serum LH concentration and in individual LH pulse amplitude with no change in LH pulse frequency. In contrast, progesterone treatment for 7 days increased LH pulse amplitude with no change in basal serum LH concentrations and a significant reduction in LH pulse frequency. We concluded that firstly, progesterone does exert a biphasic feedback effect on LH secretion and that the nature of this effect is determined by the duration of exposure to the progesterone stimulus. Secondly, as LH pulsatility has been shown to be an accurate indicator of GnRH pulsatility, that the reduction in LH pulse frequency after a long exposure to progesterone is due to a hypothalamic effect of progesterone whereas the positive feedback effect may be the result of a pituitary or hypothalamic action.
A DIRECT ASSAY FOR PROINSULIN IN PLASMA AND ITS APPLICATIONS IN HYPOGLYCAEMIA
Authors: HAMPTON S. M. , BEYZAVI K. , TEALE D. , MARKS V. 
Published: March 2008

SUMMARYA direct radioimmunoassay in unextracted plasma is described. The assay has a sensitivity of 4 pmol/l (2 standard deviation from zero). The proinsulin antiserum was immuno‐adsorbed against human C‐peptide and insulin coupled to glass beads. Cross‐reactivity of the antiserum was assessed and shown to be less than 0·01% with both peptides. In normal healthy fasting subjects the plasma proinsulin level was 6·7 ± 1·7 pmol/l (n=17) (mean ± SD). Fasting proinsulin levels in non‐insulin dependent diabetics were significantly elevated compared with non diabetics (14·2 ± 2 pmol/l (n=11) vs 6·7 ± 1·7 (n=17) P>0·005). The insulin/proinsulin ratio was 3·4:1 in the non‐insulin dependent diabetic compared with 6:1 in non‐diabetics. Samples from 21 insulinoma patients were assayed and mean fasting plasma proinsulin level was 255 pmol/l ± 479 when the patients were hypoglycaemic. The range in pro‐insulin levels was large (30–2300 pmol/l). Mean fasting proinsulin level in three hypoglycaemic subjects due to sulphonylurea overdose was 15·7 ± 2·3 pmol/l. The molar ratio of proinsulin to insulin was 1:6 in healthy subjects, 1:1 in insulinoma patients and 10:1 in sulphonylurea induced hypoglycaemic patients.
EXAGGERATED INSULIN SECRETORY RESPONSE IN PATIENTS WITH INSULINOMAS TO MIDAGLIZOLE, A DRUG WITH α2‐ADRENERGIC BLOCKING ACTIVITY
Authors: YAMADA Y. , KONO N. , HANAFUSA T. , MINEO I. , NAMBA M. , ITOH H. , KIYOKAWA H. , KAWACHI M. , YAMASAKI T. , TARUI S. 
Published: March 2008

SUMMARYMidaglizole is a new α2‐adrenergic blocking agent which increases insulin release from normal pancreatic islets. We studied its effect in four patients with insulinomas. In three patients oral administration of 150 mg of midaglizole caused a large increase in serum insulin and a corresponding decrease in plasma glucose. The magnitude of the response cannot exclude the possibility that midaglizole has direct beta cell stimulatory activity. Two of the three patients had operations, and their insulin responses to midaglizole became normal after removing the tumours. In contrast, midaglizole did not stimulate insulin secretion in the fourth patient. A midaglizole stimulation test might be useful in screening patients with insulinomas.
BASAL AND STIMULATED INSULIN LEVELS RISE WITH ADVANCING PUBERTY
Authors: SMITH C. P. , ARCHIBALD H. R. , THOMAS J. M. , TARN A. C. , WILLIAMS A. J. K. , GALE E. A. M. , SAVAGE M. O. 
Published: March 2008

SUMMARYWe studied the effect of pubertal development on insulin secretion. Intravenous glucose tolerance tests were performed on 47 islet‐cell antibody negative siblings of diabetic children and on 16 normal adults. Puberty was staged using Tanner's criteria and subjects were grouped as follows: I, stage 1 (n= 16); II, stages 2 and 3 (n=15); III, stages 4 and 5 (n= 16); IV, adults (n= 16). Fasting insulin increased with advancing puberty (p= 0.59,P< 0.001). The stimulated insulin response also rose with increasing pubertal development: for the 0‐10 min insulin area, ρ= 0.46,P<0.001 and for the 10‐60 min area,ρ=0.68,P<0.00. There was a low positive correlation between insulin and age to 16 years but multiple regression analysis showed that this could be accounted for by puberty alone. Indeed prepubertal children and adults did not differ. There was no correlation between glucose (fasting and 0‐60 min area) and puberty or age. These findings suggest that insulin resistance increases during puberty, and this may contribute to the frequency of presentation or worsening control of insulin dependent diabetes at this time.
THE CORTISOL RESPONSE TO CORTICOTROPHIN‐RELEASING FACTOR IS BLUNTED IN OBESITY
Authors: KOPELMAN P. G. , GROSSMAN A. , LAVENDER P. , BESSER G. M. , REES L. H. , COY D. 
Published: March 2008

SUMMARYAbnormalities of the adrenal cortex may be associated with extreme obesity but there is little information about hypothalamic‐pituitary function. We have investigated this by measuring plasma ACTH and Cortisol responses to ovine corticotrophin releasing factor (CRF‐41), 0.5 μg/kg/body weight, in 10 obese women and seven age‐matched normal weight women. The Cortisol response to insulin‐induced hypoglycaemia and intravenous synacthen (2.5 ng/kg/body weight) were also measured on different occasions in some of the subjects. The peak ACTH response to CRF was less in the obese but this was not significant (obese ACTH ± SEM, 31 ± 4 ng/l, controls 39 ± 4 ng/1) whereas the peak Cortisol was significantly reduced in the obese (obese Cortisol, 456 ± 21 nmol/l, controls 638 ± 50 nmol/l). Doubling the dose of CRF did not significantly alter either ACTH or Cortisol responses in six of the obese patients. The peak Cortisol response to symptomatic hypoglycaemia and following i.v. low dose synacthen stimulation was similar in the obese and normal weight women. We conclude that obese women have a normal Cortisol response to hypothalamic‐pituitary stimulation by hypoglycaemia and direct adrenal stimulation by synacthen but an impaired adrenal response to pituitary stimulation with CRF. Although the explanation for these findings is uncertain, our study underlines the importance of considering an individual's body weight when assessing the Cortisol response to CRF stimulation.
RADIOIMMUNOASSAY ARTIFACT ASSOCIATED WITH CIRCULATING ANTI‐RABBIT ANTIBODIES
Authors: JEFFCOATE W. J. , SELBY C. , POWELL R. J. 
Published: March 2008

SUMMARYA 30 year old woman presenting with infertility was found to have elevated serum immunoreactive prolactin, TSH and total T3. These findings were eventually attributed to assay artifact when she was shown to have anti‐rabbit antibodies in her serum. The possibility of laboratory artifact should be considered in clinical practice when abnormal immunoassay results are unsupported by clinical or radiographic data.
THYROXINE‐BINDING GLOBULIN DEFICIENCY RE‐EXAMINED
Authors: And S. COPPING , BYFIELD P. G. H. 
Published: March 2008

SUMMARYSeven sera, previously categorised as completely deficient in thyroxine‐binding globulin (TBG) by an immunoelectrophoretic technique, were re‐examined with a sensitive ELISA method. Only one of the sera was confirmed completely deficient by ELISA. The remaining six contained 0.08‐0.19 mg/1. The protein was immunologically identical with‘normal’TBG, could bind to thyroxine and had the correct mobility in reverse‐flow electrophoresis. Complete TBG deficiency may therefore be rare.
PROLACTIN RESPONSE TO METOCLOPRAMIDE DOES NOT DISTINGUISH PATIENTS WITH HYPOGONADOTROPHIC HYPOGONADISM FROM DELAYED PUBERTY
Authors: CRISTIANO A. M. , MUNABI A. , EL SABBAGH H. , CASSORLA F. , SHERINS R. J. 
Published: March 2008

SUMMARYThe prolactin response to metoclopramide (MCP) was studied in 23 sexually immature males, 14 with isolated hypogonadotrophic hypogonadism (IHH) and nine with constitutional delayed puberty. Six of the 14 IHH patients had not been treated prior to our study, whereas eight had received long term therapy with testosterone or hCG for variable periods ranging from 1 to 20 years. We also measured the prolactin response to chlorpromazine (CPZ) in the untreated IHH men. In these untreated subjects, we observed a greatly diminished prolactin response after CPZ by comparison to that measured following MCP administration (peak 15 ng/ml, areas 86 units vs peak 43 ng/ml, area 416 units, respectively) (P<0.01). Furthermore, prolactin levels following MCP were similar in untreated (peak 43 ng/ml, area 416 units) and treated (peak 55 ng/ml, area 545 units, NS) IHH males as well as in boys with constitutional delayed puberty (peak 50 ng/ml, area 532 units, NS). In addition, responses in the three groups of patients were about half (P<0‐01) those measured in normal men (peak 81 ng/ml, area 845 units). These data indicate that, unlike CPZ, MCP is not useful in distinguishing patients with hypogonadotrophic hypogonadism from boys with constitutional delayed puberty.
CIRCULATION OF A FRAGMENT OF HAEMOGLOBIN α‐CHAIN DURING A PENTAGASTRIN‐INDUCED FLUSH IN PATIENTS WITH METASTATIC CARCINOID TUMOURS
Authors: BALKS H. J. , THIM L. , CONLON J. M. 
Published: March 2008

SUMMARYIntravenous injection of pentagastrin (0‐6 /μ g/kg body wt) into two patients with metastatic carcinoid tumours evoked a severe carcinoid flush. Analysis by reverse‐phase H P L C of acetone‐extracts of peripheral blood taken from the patients during the flush indicated the presence of a peptide identified as the residues (1‐33) fragment of the α‐chain of haemoglobin. The peptide was not detected in blood taken from the patients immediately before stimulation of the flush or in the blood of healthy subjects after pentagastrin injection. The observation is interpreted as evidence that the pentagastrin‐induce carcinoid flush is associated with the activation and possible release of a tumour protease that result in damage to erythrocytes.
EFFECTS OF LOW DOSE ORAL IODIDE SUPPLEMENTATION ON THYROID FUNCTION IN NORMAL MEN
Authors: GARDNER D. F. , CENTOR R. M. , UTIGER R. D. 
Published: March 2008

SUMMARYPrevious studies have demonstrated that short‐term oral iodide administration, in doses ranging from 1500 μg to 250 mg/day, has an inhibitory effect on thyroid hormone secretion in normal men. As iodide intake in the USA may be as high as 800 μ/d, we investigated the effects of very low dose iodide supplementation on thyroid function. Thirty normal men aged 22‐40 years were randomly assigned to receive 500, 1500, and 4500 μg iodide/day for 2 weeks. Blood was obtained on days 1 and 15 for measurement of serum T4, T3, T3‐charcoal uptake, TSH, protein‐bound iodide (PBI) and total iodide, and 24 h urine samples were collected on these days for measurement of urinary iodide excretion. TRH tests were performed before and at the end of the period of iodide administration. Serum inorganic iodide was calculated by subtracting the PBI from the serum total iodide. We found significant dose‐related increases in serum total and inorganic iodide concentrations, as well as urinary iodide excretion. The mean serum T4 concentration and free T4 index values decreased significantly at the 1500 μg/day and 4500 μg/day doses. No changes in T3‐charcoal uptake or serum T3 concentration occurred at any dose. Administration of 500 μg iodide/day resulted in a significant increase (P<0.005) in the serum TSH response to TRH, and the two larger iodide doses resulted in increases in both basal and TRH‐stimulated serum TSH concentrations. Thus, iodide supplementation within the range of normal daily intake in the USA has a significant inhibitory effect on thyroid hormone secretion in normal men.
COMPARISON OF METHIMAZOLE, METHIMAZOLE AND SODIUM IPODATE, AND METHIMAZOLE AND SATURATED SOLUTION OF POTASSIUM IODIDE IN THE EARLY TREATMENT OF HYPERTHYROID GRAVES’DISEASE
Authors: ROTI E. , ROBUSCHI G. , GARDINI E. , MONTERMINI M. , SALVI M. , MANFREDI A. , GNUDI A. , BRAVERMAN L. E. 
Published: March 2008

SUMMARYWe have evaluated three regimens for the rapid control (10 days’therapy) of thyrotoxicosis in hyperthyroid Graves’disease: methimazole (MMI, 40 mg/ day), MMI and sodium ipodate (MMI + Na Ipodate, 1 g/day and MMI and saturated solution of potassium iodide (MMI + SSKI, 6 drops twice daily). When serum T4 and T3 concentrations were analysed as the percent change from pre‐treatment values, the following results were observed. Serum T4 concentration decreased in the three treatment groups and the decrease was similar in the MMI and MMI + SSKI groups but significantly lower than in the MMI + Na ipodate group. The serum T3 concentration decreased to the normal range in all seven MMI + Na Ipodate treated patients by the fourth day of treatment and the per cent decrease in serum T3 from pre‐treatment values was significantly greater than in the MMI and MMI + SSKI treated patients. The decrease in serum T3 was similar in the latter two groups. Heart rate decreased in all three groups, but the decrease was significantly more in the MMI+Na ipodate treated patients. The present findings suggest that the rapid control of hyperthyroid Graves’disease is similar in patients treated with MMI and MMI + SSKI and that the combination of MMI + Na Ipodate is more efficacious since the decrease in serum T3 concentrations and heart rate was significantly greater in the MMI + Na ipodate‐treated patients.
FINE ADJUSTMENT OF THYROXINE REPLACEMENT DOSAGE: COMPARISON OF THE THYROTROPHIN RELEASING HORMONE TEST USING A SENSITIVE THYROTROPHIN ASSAY WITH MEASUREMENT OF FREE THYROID HORMONES AND CLINICAL ASSESSMENT
Authors: CARR D. , MCLEOD D. T. , PARRY G. , THORNES H. M 
Published: March 2008

SUMMARYThyroxine replacement therapy for 21 adult patients with primary hypothyroidism was adjusted to the dosage at which each patient had a normal thyrotrophin (TSH) response to thyrotrophin releasing hormone (TRH). Clinical assessment and measurement of TSH (by sensitive immunoradiometric assay), free thyroxine (FT4) and free tri‐iodothyronine (FT3) were made at this dosage and at higher and lower doses of thyroxine. Clinical observations, FT3 and FT4 assays were relatively insensitive to small alterations of thyroxine dosage, in contrast to which basal TSH measurements correlated well with TRH responsiveness and were sensitive to fine adjustments of thyroxine dosage.
THE SIGNIFICANCE OF THE INITIAL FT4‐INDEX FOR THE MANAGEMENT OF SINGLE DAILY DOSE METHIMAZOLE TREATMENT OF HYPERTHYROIDISM
Authors: ARNTZENIUS A. B. , ELTE J. W. F. , FRÖLICH M. , HAAK A. 
Published: March 2008

SUMMARYSince the effectiveness of 30 mg methimazole in a single daily dose in gaining initial control of hyperthyroidism may depend largely on patient characteristics, 52 patients (34 with diffuse and 18 with nodular goitre) were investigated in an attempt to determine the relative importance of a number of pretreatment variables. Return to normal thyroid hormone levels after 2 to 6 weeks of treatment appeared to be the rule, although eight of these patients formed notable exceptions (6‐20 weeks). The individual duration of treatment until achievement of biochemical euthyroidism correlated with the initial free thyroxine index (r= 0.75, P<0.001) and the free triiodothyronine index (r= 0.70, P< 0.001). For patients with a diffuse goitre it was also related to the thyroid volume estimated by ultrasound (r= 0.73, P< 0.001). According to multiple linear regression analysis however these variables were found to have no independent prognostic value. The decrease in thyroid volume during initial therapy, the nature of the goitre, a medication compliance score and various other patient variables did not correlate with the effect of treatment. In 12 cases perchlorate discharge tests were performed. The results suggest continued hormone synthesis in patients with highly active iodine trapping as an important mechanism of the postponed attainment of euthyroidism.
RESTORATION OF NORMAL THYROTROPHIN SECRETION REDUCES THE ABNORMALLY HIGH SERUM GLUTATHIONE S‐TRANSFERASE LEVELS FOUND IN PATIENTS RECEIVING THYROXINE REPLACEMENT THERAPY
Authors: GOW S. M. , CALDWELL G. , TOFT A. D. , SWEETING V. M. , BECKETT G. J. 
Published: March 2008

SUMMARYThe peripheral tissue thyroid status of 12 patients receiving thyroxine replacement therapy was investigated both when pituitary secretion of TSH was suppressed and later, when on a lower dose of thyroxine that restored thyrotroph responsiveness. Heart rate and various analytes in serum known to be sensitive to thyroid status were measured in addition to TSH by immunoradiometric assay. Initially, the serum T4 concentration was raised in seven patients and free T4 raised in nine; all patients had normal T3 concentrations. Later, on the lower dose of thyroxine, most patients had concentrations of thyroid hormones within reference limits. Concentrations of the liver‐specific form of glutathione S‐transferase (GST) in serum decreased (P< 001) after the reduction in thyroxine dose; abnormally high GST levels, found in eight patients when TSH was suppressed, returned to normal in six of these patients when normal basal and TRH‐stimulated TSH concentrations had been restored. The response of the pituitary to excess thyroxine may be more representative of other tissues (e.g. the liver) than previously thought.
THE EFFECT OF OXYTOCIN INFUSION ON ADENOHYPOPHYSIAL AND ADRENAL CORTICAL RESPONSES TO INSULIN‐INDUCED HYPOGLYCAEMIA
Authors: NUSSEY S. S. , PAGE S. R. , ANG V. T. Y. , JENKINS J. S. , WHITE A. 
Published: March 2008

SUMMARYThe responses of plasma adrenocorticotrophin (ACTH), Cortisol, growth hormone (GH) and prolactin to insulin‐induced hypoglycaemia were studied in six lean male subjects (age 22‐29 years). Intravenous insulin tests were performed with and without oxytocin infusion. Blood sugar nadir occurred at the onset of symptoms (time S) with no significant differences between oxytocin and saline infusion. During the oxytocin infusion mean plasma oxytocin increased from 1.9 pmol/l to 138 pmol/l. Peak increase in plasma ACTH (oxytocin 266 ± 54 ng/l; saline 281+43 ng/l, mean + SEM) was at S +10 min while peak plasma Cortisol (oxytocin 680± 47 nmol/l: saline 656 ± 40 nmol/l) was measured at S ± 60 min, peak GH (oxytocin 96+17.8 mU/l; saline 106 ± 18.6 mU/l) at S + 60 min and prolactin (oxytocin 1332 ± 239 mU/l; saline 1242 ± 273 mU/l) at S + 30 min. There were no significant differences in plasma concentrations of ACTH, Cortisol, GH or prolactin between saline and oxytocin infusion. The results indicate that oxytocin has no effect on plasma ACTH, Cortisol, GH and prolactin responses to insulin‐induced hypoglycaemia. In particular they fail to support previous studies which suggested an inhibitory role for oxytocin in ACTH secretion.