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Twenty British Friesian steers were divided into four uniform groups and either not treated or implanted with hexoestrol, trenbolone acetate, or hexoestrol plus trenbolone acetate. Hexoestrol was given 90 days and trenbolone acetate 70 days, before slaughter. Animals in the treatment groups grew significantly faster, converted food to live-weight gain more effciently faster, converted food to live-weight gain more efficiently and had lower levels of plasma urea and to a lesser extent serum albumin than untreated controls for the final 70 days before slaughter. The combined treatment of hexoestrol plus trenbolone acetate produced more pronounced effects than either compound given alone. Steers treated with hexoestrol had significantly greater levels of serum growth hormone than steers implanted with trenbolone acetate alone or untreated controls, but the treatments had no significant effect on levels of plasma glucose, free fatty acids or serum insulin. Carcase conformation and fat cover assessed subjectively did not differ between treated and control animals but killing out percentage was generally higher in all treatment groups.

SUMMARY. Serum growth hormone (GH) behaviour after levodopa administration was measured in twelve healthy subjects both in basal conditions and after a 4 day course of pimozide (4 mg daily), a specific blocker of dopamine (DA) receptors. In addition, fasting plasma GH was measured on the first, second and third day of treatment. No significant difference was found between GH response to levodopa in basal conditions and after pimozide; moreover, fasting GH was uninfluenced by pimozide.

Electrical stimulation of hypothalamic “feeding areas” (VMH & LHA) through stereotaxically implanted electrodes was carried out in normal and streptozotocinized diabetic conscious male rhesus monkeys. In normal monkeys, the VMH stimulation resulted in a significant decrease in serum insulin and blood glucose while opposite responses were observed following LHA stimulation. Serum growth hormone, FFA and plasma cortisol levels increased significantly on stimulation of LHA and VMH in normal animals. The pattern of blood glucose and serum growth hormone responses to stimulation of “feeding areas” was similar in normal and diabetic animals. The serum insulin, FFA and plasma cortisol were largely unaffected while growth hormone increased significantly by stimulation of these areas in diabetes. The present study indicates that the stimulation of “feeding areas” does not alter the diabetic syndrome significantly nor does diabetes prevent the changes in metabolism seen after stimulation of “feeding areas.”

Growth hormone (GH) was measured by radioreceptorassay (RRA) and radioimmunoassay (RIA) in the sera of 24 children with idiopathic primary growth retardation (PGR), 15 with genetic short stature (GSS) and 11 with intra-uterine growth retardation (IUGR), and compared to results obtained in normal children. The average RRA/RIA ratio was close to normal in PGR (1.02 ± 0.05) and in IUGR (1.06 ± 0.07), and slightly though not significantly lower in GSS (0.86 ± 0.06). Some variability in RRA/RIA ratio was found in individual patients of each group, and some sera gave a non-parallel displacement of the tracer when compared to the standard curve. But no genetic difference of RRA-assayable GH was found between the three groups studied and normal children.

To demonstrate the effect of diazepam on serum growth hormone and prolactin levels in acromegaly, 7 acromegalics were studied. Every patient received 10 mg diazepam orally at zero time, and blood samples were obtained at 30-min intervals. The same patients also underwent a standard L-dopa test. They were given 500 mg L-dopa orally at zero time, and blood samples were obtained at 30-min intervals. The administration of diazepam did not induce any significant changes in either growth hormone or prolactin levels. On the other hand, the administration of L-dopa resulted in a significant decrease in growth hormone level from 74.25 +/- 22 ng/ml (mean +/- SEM) at zero time to a level of 52.8 +/- 21 and 58.77 +/- 22.7 ng/ml at the 60- and 90-min intervals, respectively (p less than 0.05), and a significant decrease in prolactin level from a baseline of 56.18 +/- 17 to 25.5 +/- 8.4 ng/ml (p less than 0.001) at the 60-min interval. It is suggested that the response of growth hormone to diazepam in acromegalics is qualitatively different from nonacromegalic controls.

Because of the increasing use of morphine anesthesia for open-heart surgery and the known ability of the drug to inhibit ACTH release, we have studied the effect of morphine anesthesia on plasma cortisol and growth hormone response to major surgery. In patients receiving 1 mg/kg morphine anesthesia the normal rise in plasma cortisol in response to major abdominal surgery was suppressed. This was also true in patients receiving 4 mg/kg morphine as anesthesia for open-heart surgery. In the latter group the normal rise in serum growth hormone was suppressed as well. This suppression of cortisol and growth hormone response during morphine anesthesia caused no clinically observable ill effect and could be reversed with ACTH.

A sensitive and reproducible radioreceptor assay (RRA) for human growth hormone (HGH) is described. It allows the evaluation of HGH concentrations as low as 2 ng/ml. It has a limited cross-reactivity with human prolactin, which does not interfere at physiological levels in children. Comparison of the results with those of radioimmunoassay (RIA) showed no discrepancies in the serum of normal children before and after stimulation tests for GH (mean RRA/RIA ratio 1.03 ± sem 0.04, range 0.75 to 1.65) nor in the serum from hypopituitary dwarfs during the 12 h following an im injection of 6 mg of HGH (mean RRA/RIA ratio 1.05 ± sem 0.04, range 0.84 to 1.28). It is concluded that receptoractivity of HGH is parallel to its immunoreactivity in normal children and in hypopituitary patients receiving clinical grade HGH.

To follow growth of rats, in which growth hormone secretion has been chronically stimulated, l -Dopa (5 mg/kg) was injected subcutaneously twice daily for 70 days to growing rats. A control group, matched for sex and sibship, pair fed with the treatment group was given saline injections. At 10-day intervals, the rats were weighed and measured. At 90 days of age the rats were ether anesthesized, bled for growth hormone determination, and internal viscera weighed. Weight gain and length in the l -Dopa-treated group was found to be significantly greater. A mean weight gain of 6% and 12% in the male and female rats, respectively, and a mean length gain of 5% in both male and female rats was observed at 90 days of age. The thymus, thyroid, adrenals, uterus, and gonads all tended to be heavier in the l -Dopa-treated group. Significantly heavier kidneys were found in the l -Dopa group. Serum growth hormone was found to be 8.44 ± 1.4(SE) ng/ml in the l -Dopa group and 4.6 ± 0.9 ng/ml in the control group. It is concluded that the continuous administration of l -Dopa produces an increase of circulating serum growth hormone levels, and this in turn enhances growth.

Chemical diabetes is an incompletely defined form of glucose intolerance which is more common in the later decades of life. Long-term observations indicate that in half of the patients with persistent chemical diabetes, overt diabetes mellitus develops in the course of one decade of aging. Other studies have established that chemical diabetes is characterized by hyperinsulinemia which may be preceded by an initial lag in the insulin responses to oral administration of glucose. As a group, persons with chemical diabetes manifest higher serum triglyceride levels, a greater frequency of electrocardiographic abnormalities, and increased proteinuria. The data presented describe growth hormone patterns in chemical diabetes. The findings indicate that the lower serum growth hormone levels of obese adults of all age decades are also evident during glucose tolerance tests indicative of mild or moderate chemical diabetes. However, more severe degrees of glucose intolerance and chemical diabetes in obese persons are characterized by further decreases in growth hormone indices beyond those characteristic of obesity alone.

Rarely, acromegaly is produced by neuroendocrine neoplasms elaborating a substance similar to or identical with growth hormone-releasing factor. This report reviews the cases described to date and presents the clinicopathologic features of a patient with acromegaly, mild sellar enlargement, and elevated growth hormone levels associated with a large bronchial carcinoid tumor. Normalization of serum growth hormone levels and regression of acromegaly followed resection of the bronchial tumor, which was shown, by bioassay and immunocytochemistry, to contain a growth hormone-releasing factor.

Ten schizophrenic and five epileptic patients under antipsychotic drug treatment were studied to evaluate sleep-related GH secretion. Four of the schizophrenic patients had a high secretion peak of GH (range 15.2 to 38.0 ng/ml), four had a moderate peak (range 5.8--8.3 ng/ml), while two had no increase in GH secretion during sleep (range 0.5--1.0 ng/mg). Four of the five epileptic patients had a moderately increased secretion (range 5.8--9.2 ng/ml) and one had no increase in GH secretion during sleep. Thus, the GH secretory pattern varied with the patient as in known to be also with healthy individuals. However, no clear disturbances were noted in sleep-related GH secretion in schizophrenic patients receiving antipsychotic drug treatment, when compared e.g. to non-schizophrenic, epileptic patients under a same kind of drug treatment.

Forty-four 6-mo-old, fine-wool ewe lambs were randomly allotted to one of three triiodothyronine (T(3)) treatment groups (14 or 15 ewe lambs/group). Treatments (0, 200, and 400 mug T(3)) were administered daily by subcutaneous injection during a 30-d treatment period in September. Following the treatments, ewe lambs were allowed to mate with Debouillet rams during a 34-d breeding season. Animal weights did not differ (P0.10) among treatment groups throughout the study. However, ewe lambs receiving 400 mug T(3)/d gained less (P0.05) during the treatment period than did those receiving 200 mug T(3)/d or controls. Grease fleece weights (6-mo clip) were similar (P0.10) among treatment groups. Serum growth hormone (GH) values in blood samples collected on Days 7 and 28 of the 30-d treatment were similar (P0.10) before treatments were administered and on Day 7 after treatments were administered. However, on Day 28 after treatments were administered, serum GH was lower (P0.01) in ewe lambs receiving 400 mug T(3)/d (1.5 ng/ml) than in those receiving 200 mug/d (2.1 ng/ml) or controls (2.2 ng/ml). Ovarian cyclicity was determined by monitoring serum progesterone. Forty percent of control ewe lambs were determined to have cycled during treatment compared with 20% of those receiving 200 mug T(3)/day and none of those receiving 400 mug T(3)/d (P0.10). Pregnancy rates were lower (P0.10) in ewe lambs receiving 400 mug T(3)/d (29%) compared with those receiving 200 mug T(3)/d (60%) or controls (66.7%). Day of conception, lambs born/ewe exposed, lambs born/ewe lambing, and lambs weaned/ewe lambing did not differ (P0.10) among treatments. Preweaning performance of offspring was not altered by maternal treatment with 200 or 400 mug T(3)/d (P0.10). These data indicate that 200 and 400 mug T(3)/d will not enhance GH production or improve reproductive performance of ewe lambs.

Eighteen mature (3 to 6 years) Debouillet × Rambouillet ewes (mean weight 79·2 (s.e. 21) kg) producing and nursing single offspring were randomly allotted to one of three groups to examine the influence of ovine growth hormone (oGH) on reproductive, hormonal and lactational responses of springlambing ewes. Each ewe received a daily subcutaneous injection of either 0, 5 or 10 mg oGH from day 11 through to day 20 post partum (day 0 = parturition). Treatment groups were subdivided into two pens (three ewes per pen) and food intake was monitored from day 1 through to day 20 post partum. On days 11 and 20 post partum, jugular blood samples were collected before and hourly for 8 h after treatment. Blood samples were also collected daily from day 10 through to day 21 post partum and on alternate days through to day 40 post partum. Milk production (oxytocin-induced hand milking) and fat and protein concentrations were determined 21 days post partum. Food intake did not differ before or during the treatment period (P > 0·05). Likewise, ewe and lamb weights were similar among treatment groups through to day 60 post partum (P > 0·05). Serum insulin did not differ before or after treatment on day 11 (P > 0·05); however, on day 20 before treatment, serum insulin was significantly higher in ewes receiving 5 (2·3 (s.e. 0·3) μg/I) and 10 (2·4 (s.e. 0·3) μg/1) mg oGH than in controls (1·2 (s.e. 0·3) μg/1) (P < 0·05). After treatment, no differences were detected in serum insulin among treatments on day 20 post partum (P > 0·05). Serum growth hormone (GH) was similar among groups before treatment on day 11 post partum; but by 8 h after treatment, serum GH was significantly elevated in ewes receiving 10 mg oGH (32·4 (s.e. 1·9) μg/1) compared with ewes receiving 5 (13·9 (s.e. 1·9) μg/1) or 0 (4·5 (s.e. 1·9) μg/1) mg oGH (P < 0·01). By 20 days after lambing, serum GH differed significantly among groups both before and after administration of exogenous oGH (P < 0·01). Ewes receiving 5 or 10 mg oGH produced 2·3 (s.e. 0·2) kg milk per day compared with 1·9 (s.e. 0·2) kg/day for controls (P < 0·10). Milk fat and protein concentrations did not differ significantly among treatments (P > 0·05), but total fat yield was higher in ewes receiving either dose of oGH (206 (s.e. 20) g/day) compared with control ewes (141 (s.e. 20) g/day) (P < 005). Serum progesterone remained less than 0·5 μg/1 in ewes through to day 40 post partum. A linear decrease was observed in interval from parturition to first observed oestrus as dosage of oGH increased (116, 108 and 102 (s.e. 6) days for ewes receiving 0, 5 and 10 mg oGH, respectively; P = 0·10). Administration of exogenous oGH to lactating. anoestrous ewes between days 11 and 20 post partum enhances milk production and may influence the interval to oestrus.

We investigated whether a decrease in serum growth hormone contributes to the short stature of adults with Turner syndrome by measuring the 24-hour profile of serum growth hormone in 30 patients aged 2 to 20 years. Growth hormone pulses were defined as a rise from nadir to peak that exceeded three times the intraassay coefficient of variation. Girls with Turner syndrome aged 2 to 8 years did not have statistically different growth hormone levels, peak amplitudes, and peak frequencies compared with those in age-matched controls. By contrast, girls with Turner syndrome aged 9 to 20 years had significantly decreased mean 24-hour growth hormone levels, peak amplitudes, and peak frequencies compared with those in age-matched normal girls. Patients with Turner syndrome of all ages had decreased serum somatomedin-C concentrations and delayed bone ages. We conclude that a relative deficiency of growth hormone in pubertal patients with Turner syndrome may contribute to their adult short stature.

✓ The preoperative outlook and surgical results are evaluated in 29 acromegalic patients, employing the usual serum growth hormone (GH) screening techniques in association with GH response to the thyrotropin releasing hormone (TRH) test. Results obtained by transsphenoidal microsurgical technique in adenomas of different size and sellar morphology are reported. Overall results clearly favor selective microsurgery in early diagnosed and operated tumors (microadenomas), while a less than radical approach does not hold much promise of functional normalization in larger adenomas. In nonnormalized cases the efficacy of radiotherapy is stressed. The TRH test results were a good indication for radiation therapy even in those cases in which GH normalized after surgery by common assay methods.

Insulin and propranolol-glucagon stimulation tests were carried out on 28 children and 5 adolescents and the results of their growth hormone and plasma cortisol estimations were compared. Twenty-nine subjects with normal growth hormone reserves showed a mean maximum rise of 17.4 μU/ml of serum growth hormone in the insulin test whereas the intramuscular injection of glucagon after oral premedication with propranolol produced a rise of 38.5 μU/ml. Five subjects with normal growth hormone reserves showed a reduced hormone output in the insulin stimulation tests but normal response in the propranolol-glucagon stimulation tests. Only one subject showed a poor response in the propranolol-glucagon but normal response in the insulin stimulation test. In 30 subjects with normal adrenocortical function the mean maximum increase of plasma cortisol was 15.6 μU/ml in the insulin – and 14.9 μU/ml in the propranolol-glucagon stimulation tests, respectively. Both methods are suitable for studying the pituitary-adrenocortical interrelationships. The mechanism of the release of glucagon-induced growth hormone is not clear but the fall in blood glucose does not seem to play a major role in the process. A stress-like mechanism is equally unlikely because vegetative symptoms occurred only i a small number of subjects after intramuscular glucagon administration. It is possible that glucagon possesses a releasing-like mechanism which operates in the pituitary itself.

Blood-free-fatty acids (F.F.A.) and growth-hormone levels were determined in 9 children subjected to cardiac catheterization and angiography. A significant rise of growth-hormone level was recorded immediately after angiocardiography, followed by a marked increase of F.F.A. levels 2--4 hours after termination of the catheterization. These results may indicate that the high levels of F.F.A. sustained after cardiac catheterization and angiography are probably due to the increase of growth -hormone secretion during the procedure.

In two experiments, a high dietary level of available phosphorus (.65%) in the presence of high chloride concentrations (.36%) was associated with a significant increase in the incidence of tibial dyschondroplasia (TD) in male broiler chickens. The level of dietary calcium and the interaction between Ca and available P had no effect on TD. Heterozygous normal (DW/DW) male broilers had a significantly lower incidence of TD than homozygous normal (Dw/Dw) chicks (Experiments 1 and 2). In Experiments 3 and 4, there were no significant differences between BW at 14 days for roaster-broiler cross and broiler chicks. At 21 and 28 days, however, the roaster-broiler cross chicks weighed significantly less than the broilers and had a significantly lower incidence of TD. Decreasing growth rates in broiler chicks after 14 days of age resulted in a significant decrease in the incidence of TD (Experiments 4 and 5), but did not decrease the severity of TD lesions at 28 days (Experiment 5). Depressed growth from 0 to 14 days decreased, but did not eliminate, TD lesions (45%) at 28 days, but it did significantly decrease the severity of the lesions compared with that in the 14 to 28-day manipulation treatments (Experiment 5). In Experiment 5, chicks were growth restricted from 0 to 14 or 14 to 21 days and then ad libitum fed the control diet until 28 days of age. The serum growth hormone concentrations at 28 days were inversely related to the rate of BW gain from 21 to 28 days of age, independent of BW at 21 or 28 days or feed consumption from 21 to 28 days. There were no differences in serum concentration of thyroxine or triiodothyronine at 28 days.

This study was carried out in order to determine whether children with a transitory type of growth hormone deficiency showed an accelerated growth in height velocity on treatment with human growth hormone (HGH). Following careful diagnostic routine procedures 13 extremely short children were diagnosed as having isolated growth hormone deficiency, and were successfully treated with HGH. A true isolated growth hormone deficiency was present in 5 of the children, whereas 8 showed a normal increase in serum growth hormone on repeated growth hormone stimulation tests after their development of puberty and termination of HGH treatment. Three boys with bone ages of 5.5, 8.0 and 9.5 years showed an undisputable effect following HGH administration. They showed an initial growth at the start of treatment, and a second growth spurt during development of puberty. Two of the boys reached final statures of 14 cm taller than the predicted heights. The other patients, including the children with true isolated growth hormone deficiency showed an initial spurt of growth at the start of the HGH treatment immediately followed by a pubertal growth spurt. The mean acceleration of height velocity for the children with true isolated growth hormone deficiency was from 3.4 cm during the year before treatment to 7.0 cm during the first year on treatment, as compared to 2.8 and 7.4 cm, respectively, for the children with transitory growth hormone deficiency. A girl with severe anorexia nervosa who had a transitory growth hormone deficiency, showed an accelerated high velocity from 1.1 cm to 7.6 cm during the first year following treatment with HGH. The question whether HGH treatment should be made available to all short children with no known syndrome, and presenting a height less than −3.5 sds, a bone age/chronological age ratio of less than ⅔, and a height velocity less than −2 sds is discussed. The only way to know if a child will respond to HGH treatment is to give it for a trial period of at least six months. At least a physiological stimulus to growth hormone secretion should be decisive in the selection of growth retarded children for HGH treatment. Different mechanisms seem to be responsible for physiological growth hormone secretion to sleep or exercise, and the secretion obtained with pharmacological stimuli.

A two-factorially experiment was done over a period of 42 days using 32 male, weaned Sprague-Dawley rats in order to study the effect of insufficient protein supplementation, with regard to quantity and quality (13% protein in comparison to 18%, and an essential amino acid index of 64 in comparison to 92%, resp.), on weight development and serum growth hormone concentration. Qualitative protein deficiency had a greater adverse effect on weight development and feed utilization than did quantitative protein deficiency. Both test factors combined brought about the lowest body weight and poorest feed utilization. A lowered hematocrit value occurred only after quantitative protein deficiency. The serum urea concentration was elevated after protein deficiency due to poor quality protein; the serum protein concentration tended toward reduction in both the case of qualitative as well as in the case of qualitative-quantitative protein deficiency. After providing the animals poor quality protein, growth hormone levels in serum were reduced, whereas the concurrence of both factors of protein deficiency caused the growth hormone concentration in serum to rise to a value 4.2-fold of the control value.

Several times throughout the year, changes in serum growth hormone (GH) levels over a 24-h period were determined in goldfish maintained under photoperiods and temperatures simulating natural (Edmonton) environmental conditions. In the goldfish a reproducible daily rhythm in circulating GH levels was not present at any time of the year. The average serum GH level over the daily sampling period and the instantaneous relative growth rate in goldfish sampled at the various times of the year were also determined. The highest mean daily serum GH levels were found in March and June, whereas the lowest level was found in goldfish sampled in November. Changes in mean daily serum GH levels were closely correlated to seasonal changes in daylength. The highest growth rate was found in goldfish sampled in July, whereas the lowest growth rates were found in February and March. Female goldfish exhibited a faster growth rate than male goldfish at certain times of the year, but sexual differences in growth rate were correlated with sexual differences in serum GH levels only in November when female goldfish had a higher serum GH level than male goldfish.

A series of experiments was conducted to examine the response of neonatal, male broiler chicks to brooding at a reduced temperature. In Trials 1 and 2, chicks brooded at 26.7 C generally had lower body weights and higher serum corticosterone levels during the first week after hatch than those brooded at 32.2 C. However, significant differences in body weight were observed only on Day 6 in Trial 1 and on Days 1 and 5 in Trial 2. Serum corticosterone levels, likewise, were not significantly different on all days in Trials 1 and 2. These hormone levels were statistically different on Days 1 and 5 in Trial 1 and on Days 1 and 3 in Trial 2. Brooding neonates at 26.7 C for 3 days in Trials 3 and 4 resulted in consistently lower body weights and gain and higher serum corticosterone, thyroxine, total protein, albumin, and globulin. Serum growth hormone levels in chicks brooded at 26.7 C were initially depressed the first day but were elevated on the 2 subsequent days, compared with chicks brooded at 32.2 C. Considering the physiological importance of corticosterone and thyroxine in the adaptation of chickens to cold environmental temperatures, it would be useful to evaluate the genetic variation associated with the responsiveness of these hormones in a randombred population and to improve tolerance of neonatal chickens to reduced temperature brooding through selection.

Fasting serum growth hormone values of infants and some children with thedeprivation syndrome were increased, providing tests were done before unrestricted feeding. Pituitary growth hormone and adrenocorticotropic hormone release were unresponsive to hypoglycemia only in children (5/7); however, some (3/5) had normal or increased serum growth hormone values on admission, and all had normal metyrapone tests. One severely emaciated child probably had deficient growth hormone and thyroid function. Control infants with growth failure due to undernutrition with an organic basis had elevated fasting serum growth hormone values. Insensitivity to hypoglycemia was not related to the severity of the linear growth failure and probably does not reflect growth hormone deficiency at the target organ.

Sprague-Dawley rats at birth were redistributed among nursing mothers, 4 to some, 16 to others. After 21 days, they were studied by sex and by nutritional state using a heterologous radioimmunoassay for growth hormone (GH) content of pituitary gland and plasma. Greater access to milk resulted in mean body weights of males and females of 63 ± 1 g contrasting with 34 ± 2, p < 0.01,and pituitary weights of 3.0 ± 0.07 mg, contrasting with 2.0 ± 0.06, p < 0.01. Better nutrition was attended by plasma GH of 34 ± 14 ng/ml, in contrast to 14 ± 2 ng/ml in the undernourished. There were highly significant differences in total pituitary growth hormone (257 ± 12 μg/gland in well-fed; 88 ± 6 μg/gland in the undernourished). During two weeks of free access to food, the rats from the 16 per mother group grew at 5 times their previous rate (7.5 g per day vs 1.5 g) and nearly overtook the previously better-fed group; plasma growth hormone with dietary repletion was the highest observed, and pituitary weights and growth ho...

The serum growth hormone response to a very mild, but prolonged exercise load – 225 kgm/min for 60 minutes – has been studied in 6 young non-obese healthy male subjects and 6 young obese healthy male subjects. The exercise load was easily tolerated by all subjects, and pulse rates at rest and during exercise were not much different in the two groups. The exercise-induced growth hormone rise in the non-obese subjects was discernible 30 minutes after start of work, and the maximum value of 26 ng/ml was reached 10 minutes after cessation of work. In contrast, no rise at all was seen in any of the obese subjects. It is thus demonstrated that exercise is similar to other growth-hormone-releasing stimuli: their potency is reduced in obesity.

SummaryJugular blood was collected from 34 Holstein heifers from 26 days before parturition until 26 days postpartum or until first estrus. Serum prolactin varied between 80 and 110 ng/ml until Day 2 prepartum when it increased markedly to peak of 285 ng/ml at 1 day prepartum. Prolactin decreased linearly (p < 0.01) from the peak until 2 days after calving, stabilized at about 90 ng/ml until Day 9, and gradually declined until day 26 (36 ng/ml). Postpartum (Day 5-26) prolactin was lower (p < 0.05) than prepartum (Day 26-5) prolactin. Growth hormone followed a pattern similar to prolactin but peaked 24 hr later, at parturition, and decreased from the peak to concentrations characteristic of prepartum values by Day 4 postpartum. Serum growth hormone during late pregnancy (Day 26-5) was lower (p < 0.05) than during early lactation (Day 5-26). Serum LH was consistently low (0.4-0.8 ng/ml) until Day 9 postpartum when it increased to about 1.5 ng/ml until first estrus.

Sixteen uremics with normal fasting blood glucose were studied. Abnormal glucose tolerance was a frequent finding. The initial insulin response to glucose was normal. Ten out of the 15 uremics studied with oral glucose exhibited a paradoxical rise in serum growth hormone. These uremics were significantly more intolerant to glucose than their counterpart with normal growth hormone response.

Effect of TRH administration on serum TSH and GH was studied in 9 normal subjects and 11 patients with acromegaly or gigantism. TRH provoked a prompt increase of serum TSH in normal subjects, whereas no appreciable change of serum GH was observed. Serum TSH responses to TRH were lower in most of the patients, but 8 out of the patients showed a remarkable increase of serum GH within 30 min after TRH injection. These results appear to indicate that specificity of TRH is not absolute in the functioning pituitary tumor secreting GH.

Juvenile diabetics and normal subjects were studied during different exercise loads, and juvenile diabetics were studied with half-hourly blood sampling during day-time. The growth hormone response to exercise in normals, the growth hormone hyperresponse to exercise in juvenile diabetics, and the growth hormone hypersecretion during day-time in juvenile diabetics were not diminished when the exercise-induced fall in free fatty acids in normals and diabetics and the fluctuations in the day-time free fatty acid level in diabetics were prevented by intravenous infusion of Intralipid and heparin, resulting in serum-free fatty acid levels 3-7 times higher than normal. A feedback mechanism between free fatty acids and growth hormone could not be demonstrated.

Serum growth hormone was studied during a mild exercise load of 350 kgm. per minute for twenty minutes in four groups of subjects: nonobese normal subjects, obese normal subjects, nonobese maturity-onset diabetics and obese maturity-onset diabetics. It was found that (1) the fasting pre-exercise serum growth hormone level was higher and the exercise response occurred earlier and was greater in diabetics than in normal subjects; (2) in the nonobese groups, the basal values and exercise responses in diabetics were significantly different from those of normal individuals. In the obese groups, the mean exercise response was higher in diabetics than in normals, but this difference was not significant; the basal values were identical in the two groups; and (3) the basal values and exercise responses were higher in nonobese diabetics than in obese diabetics. In normal subjects, the exercise responses were higher in the nonobese group than in the obese group.

A modification of the chromatographic method for determination of growth hormone using vertical »dry« chromatography with Whatman 3 MC paper is described. This inexpensive and rapid technique gives a better separation of free from antibody-bound growth hormone than previously published chromatographic techniques. It also gives good reproducibility, with an average recovery percentage of 104. There are high values in acromegalics and unmeasurable values in hypophysectomized patients. The values obtained are independent of antibody concentration.

The serum growth-hormone response to insulin-induced hypoglycemia has been measured in control subjects and patients with dwarfism of various causes. The normal response has been defined and applied to the assessment of growth-hormone function in patients with growth retardation. Definitive evaluation of growth-hormone responsiveness was possible in 58 of 59 patients with dwarfism.

The tall stature in patients with the XYY syndrome might be partly due to an increased production of testosterone. Fasting serum growth hormone, serum growth hormone response to an oral glucose load, and urinary excretion of pituitary gonadotrophin as well as of total and fractioned 17-ketosteroids were studied in six patients with the XYY syndrome. No significant abnormalities were found.

Increases in serum growth hormone which characterize acute starvation in non-obese individuals were usually absent in anorexia nervosa. Serum LH was decreased with serum FSH apparently normal in the majority. Increased adrenocortical activity as indicated by high basal 11 (OH)-corticosteroids and their incomplete suppression by dexamethasone and hyperresponsiveness to exogenous ACTH was recorded in about one-half of the patients tested. Urinary steroid responses to intravenous metyrapone were normal in all but one patient who had hypothalamic-pituitary hypofunction. Thyroid function was normal but TSH shortage has been reported. Resistance to insulin and a waning of insulin responses to hyperglycemia were noted in these individuals with anorexia nervosa.

To minimize methodologic artefacts, the responses of uremic patients to oral carbohydrate and to i.v. tolbutamide were evaluated in terms of increments and decrements in blood glucose and serum insulin. Uremic patients develop greater increments in blood glucose following oral carbohydrate. However, their insulin increments after oral glucose equal those of healthy controls but are not proportional to the rise in blood glucose. This indicates a flagging or waning of insulin levels relative to the hyperglycemia. In uremia i.v. tolbutamide generally produces greater increments in serum insulin and greater decrements in blood glucose. Uremic patients tend to have higher levels of serum growth hormone prior to and during oral glucose tolerance tests.

A case of Russell's diencephalic syndrome of early childhood is presented and the world literature reviewed. Assays of serum growth hormone (HGH) and fat mobilizing substance (FMS) were performed and gave very abnormal results. The role of these two substances is discussed and their value in the diagnosis of this syndrome is emphasized.

Groups of male nonobese juvenile diabetics with recent onset, short term (1-8 yr), and long-term (12-30 yr) diabetes as well as comparable nondiabetic controls were studied during exercise experiments. The chosen exercise load, 450 kg/min for 20 min never induced changes in serum growth hormone in our nondiabetic control subjects. THE PRINCIPAL RESULTS OF THE STUDY WERE AS FOLLOWS: (a) an immediate high rise in serum growth hormone followed the commencement of exercise in all diabetics. The increase and pattern of serum growth hormone was not related to the duration of the diabetes. (b) The abnormal growth hormone response to exercise in diabetics was observed when the patients were in poor control as well as when they were in clinically excellent control (fasting blood glucose level between 100 and 140 mg/100 ml). (c) However, the abnormal serum growth hormone response was significantly diminished when exceedingly strict control was achieved (fasting blood glucose level between 60 and 100 mg/100 ml). In two of these experiments an entirely normal growth hormone pattern was obtained. (d) The change in serum growth hormone pattern during regulation was totally unrelated to the changes in serum free fatty acid patterns. A normal free fatty acid level and exercise pattern was obtained much earlier during the improved control. (e) Fasting serum growth hormone levels were also significantly raised in the juvenile diabetics irrespective of the diabetes duration. (f) Fasting serum growth hormone levels were also significantly decreased during regulation. Furthermore, a significant correlation between blood glucose and fasting serum growth hormone concentration was established. (g) In the juvenile diabetics a significant increase in serum insulin was observed at the point of time when exercise was concluded.

Serum growth hormone (HGH) levels have been estimated in hourly samples for 24 hours in 2 women and 1 man. The highest levels in all subjects were found in association with the onset of sleep at whatever time that occurred. Other spontaneous peaks were found particularly in 1 woman. The rise in serum HGH levels in women following the stimuli of exercise or Bovril was greater or more rapid when these stimuli were applied mid-morning compared with early in the morning. Serum HGH levels at the same times on different days showed a great variation in the mid-morning levels from day to day in a female subject. No such variation was found in a man, nor in the female subject in the early morning.

Serum growth hormone response to hypoglycemia in man following insulin administration, reviewing lumped parameter model

Diabetes mellitus of juvenile or adult onset under treatment with insulin is characterized by higher serum growth hormone levels prior to and during disposal of an oral glucose load. The possible role of such growth hormone excesses in diabetic microangiopathy is discussed.

Serum levels of growth hormone (fasting levels, during hypoglycaemia, hyperglycaemia and after arginine infusion) were measured in acromegalic patients before (n = 35) and periodically after surgical treatment (n = 25), i.e. transethmoidal-transsphenoidal (n=20) or transfrontal pituitary ablation (n = 5). The results demonstrate that the estimation of HGH in different function tests is of high value not only for diagnosis of acromegaly but also for the assessment of the effectiveness of therapy. In pituitary adenomas with predominantly intrasellar growth the transethmoidal-transsphenoidal approach is effective to eliminate the pituitary tumor and to restore an approximately normal secretion of HGH. On the other hand, after transfrontal intervention used in some cases of larger tumours with suprasellar extension unsatisfactory results were observed with regard to the secretion of HGH.

Pituitary weight, pituitary mitotic index and pituitary and serum concentrations of growth hormone and prolactin were measured at 14‐day intervals in male rats given 10 mg diethylstilboestrol dipropionate SC every 14 days for a total period of 70 days. Mean pituitary weight reached a maximum of 21 mg on day 42 and no pituitary gland became a tumour according to a criterion of weight greater than 30 mg. Mitotic index was greatly increased until day 70 when it diminished significantly. Pituitary concentration of growth hormone decreased to maintain a low constant level from day 28 onwards while pituitary prolactin concentration rose to a maximum on day 42. Serum growth hormone was elevated on day 14 and then gradually diminished, while serum prolactin continued to increase until day 42. Pituitary weight and serum prolactin were significantly correlated and pituitary mitotic index was negatively correlated with pituitary growth hormone concentration. The state of apparent equilibrium in mass reached by the pituitary glands from day 42 until day 70, despite greatly increased secretory and mitotic activity, suggests that further disturbance of pituitary function is necessary to bring about net gain in cell numbers and lead to tumour formation.

The serum growth hormone (GH) response to insulin-induced hypoglycemia of 10 thyrotoxic patients was compared with that of 14 normal subjects. All thyrotoxic subjects had a distinct rise in GH, attaining a value of at least 6.4 ng/ml. Mean GH levels of thyrotoxic subjects did not differ significantly from those of normals at any time during the insulin tolerance test. These results indicate that GH response to insulin-induced hypoglycemia in thyrotoxicosis is normal.