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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Blood samples were taken from 30 chronically catheterized pig fetuses in utero. Levels of growth hormone, insulin, cortisol, thyroxine and somatomedin-C/IGF-1 were measured in the plasma of intact fetuses and the plasma of thyroidectomized fetuses at various gestational ages during the latter part of pregnancy. 2. Growth hormone levels were high (mean +/- SEM: 83 +/- 9 ng/ml and remained constant throughout this period. 3. Insulin levels were also constant and ranged between 4 and 14 mU/l. 4. Cortisol levels showed a general increase from 400 nmol/l at 97 days to 1200 nmol/l at term and this increase was not affected by thyroidectomy. 5. IGF-1 levels were lower than in the sows (48.0 +/- 3.0 ng/ml) and did not change throughout this period. 6. Thyroxine levels were also unchanged at about 92 +/- 4 nmol/l. 7. Thyroidectomy resulted in lower (P less than 0.001) thyroxine levels (28 +/- 3 nmol/l) but had no effect on the levels of any other hormone.
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PMID:Changes in the levels of growth hormones, insulin, cortisol, thyroxine and somatomedin-C/IGF-1, with increasing gestational age in the fetal pig, and the effect of thyroidectomy in utero. 257 61

We have investigated whether the previously demonstrated stimulatory actions of growth hormone on DNA synthesis and (pro)insulin biosynthesis and release of isolated adult rat islets of Langerhans are mediated by an autocrine release of somatomedin-C/insulin-like growth factor I (SM-C/IGF I). In medium containing 1% fetal calf serum, the presence of 16.7 mmol/l glucose, or 2.7 mmol/l glucose supplemented with a concentrate of essential amino acids, caused a significant increase in 3H-thymidine incorporation and insulin release compared to 2.7 mmol/l glucose alone but no increase in SM-C/IGF I release. Further supplementation with 1 microgram/ml growth hormone increased 3H-thymidine incorporation and SM-C/IGF I release within all groups, and insulin release in the 16.7 mmol/l glucose and 2.7 mmol/l plus amino acid groups. The ability of growth hormone to increase 3H-thymidine incorporation in the presence of 16.7 mmol/l glucose, but not its action on insulin release, was partly inhibited by a monoclonal antibody against SM-C/IGF I (control cultures 100%; growth hormone alone 261 +/- 27%, mean +/- SEM; growth hormone + anti-SM-C/IGF I 179 +/- 21%; p less than 0.05, n = 18). Growth hormone, but not 100 ng/ml SM-C/IGF I, increased insulin biosynthesis assessed as immunoprecipitable 3H-labelled insulin by 45%, but this was accompanied by a similar increase in overall protein synthesis. Similarly growth hormone, but not SM-C/IGF I caused a 75% increase in glucose oxidation by islets. Both growth hormone and SM-C/IGF I failed to increase the cellular uptake of alpha-aminoisobutyric acid or 3-O-methyl glucose over a 90 min period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Growth hormone regulation of DNA replication, but not insulin production, is partly mediated by somatomedin-C/insulin-like growth factor I in isolated pancreatic islets from adult rats. 266 10

Growth hormone is reported to increase renal plasma flow (RPF) and glomerular filtration rate (GFR) in some but not all studies. The discrepant results could be due to a delay in the effects of growth hormone on renal function. We therefore examined whether a growth hormone injection does increase RPF and GFR, whether this increase is delayed, and whether elevation in RPF and GFR is associated with increased plasma levels of insulin-like growth factor I (IGF-I). Seven normal adults received a single intramuscular injection of growth hormone, 0.15 mg/kg, and serial PAH and inulin clearances were then monitored for three consecutive days. Plasma growth hormone levels peaked an average of 2.25 hours after injection, at 128 +/- 12 SEM ng/ml, and then began to decrease; on the second day values were only slightly elevated and on the third day they were not different from baseline. Plasma IGF-I, analyzed by direct radioimmunoassay, did not change on the first day during 5.5 hours of measurements after injection. By the second day, plasma IGF-I was elevated to over twice baseline levels (P less than 0.05) and remained elevated on the third day (P less than 0.05). RPF and GFR did not change from baseline (546 +/- 19 and 100 +/- 3 ml/min/1.73 m2, respectively) during the 5.5 hours after injection on the first day.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The delayed effect of growth hormone on renal function in humans. 270 79

Growth hormone (GH) secretory patterns were studied in a patient with ectopic growth hormone releasing factor (GRF) secretion and in normal men given continuous infusions of human growth hormone releasing factor (1-40)-OH (hGRF-40). In the patient with ectopic GRF secretion, GH secretion was pulsatile despite continuously elevated immunoreactive GRF levels. To determine if pulsatile GH secretion is maintained in normal subjects, we administered to six healthy young men vehicle or hGRF-40, 2 ng/kg per min, for 24 h and gave a supramaximal intravenous bolus dose of hGRF-40, 3.3 micrograms/kg, after 23.5 h of infusion. hGRF-40 infusion resulted in greater GH secretion than did vehicle infusion and pulsatile GH secretion was maintained throughout hGRF-40 infusion. During the 23.5 h of vehicle infusion, total GH secretion (microgram; mean +/- SEM) was 634 +/- 151 compared with 1,576 +/- 284 during hGRF-40 infusion (P = 0.042). The GH response to the intravenous bolus of hGRF-40 was greater after vehicle infusion than after hGRF-40 infusion; 877 +/- 170 and 386 +/- 125 micrograms of GH was secreted after the bolus on vehicle and hGRF-40 days, respectively (P = 0.015). The total amount of GH secreted during the 25.5 h of the two study days was not different; 1,504 +/- 260 and 1,952 +/- 383 micrograms were secreted during vehicle and hGRF-40 days, respectively (P = 0.36). Not only was pulsatile GH secretion maintained during hGRF-40 infusion, but there was augmentation of naturally occurring GH pulses, which is in contrast to the effect of gonadotropin-releasing hormone on gonadotropin secretion. We suggest that GH pulses are a result of GRF secretion that is associated with a diminution or withdrawal of somatostatin secretion.
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PMID:Pulsatile growth hormone secretion in normal man during a continuous 24-hour infusion of human growth hormone releasing factor (1-40). Evidence for intermittent somatostatin secretion. 286 Jan 26

Growth hormone (GH) responses to growth hormone-releasing factor (GRF) were evaluated in 55 children with growth failure. The study groups consisted of group 1, severe GH deficiency; group 2, partial GH deficiency; group 3, patients with prior cranial radiation for nonpituitary brain tumors; and group 4, children with idiopathic growth failure. Children in group 1 were unresponsive to GRF (mean GH peak +/- SEM, 1.6 +/- 0.5 ng/ml). Higher GH responses to GRF were observed in both groups 2 (17.2 +/- 4.1 ng/ml) and 3 (10.4 +/- 2.8 ng/ml). The highest GH responses to GRF were observed in group 4 (35.9 +/- 4.3 ng/ml). ANOVA revealed a significant difference between groups (F = 12.9; df = 3; p less than 0.01), and further analysis by the Scheffe and Student-Newman-Keuls tests revealed that group 4 was significantly higher than groups 1, 2, or 3 (p less than 0.05). These data suggest that GRF unresponsiveness is a reliable predictor of severe GH deficiency. In patients with partial GH deficiency or idiopathic growth failure, the GRF gives semiquantitative information about somatotrope responsivity to exogenous stimulation.
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PMID:Diagnostic value of the growth hormone-releasing factor stimulation test. 313 44

Growth hormone (GH) was measured before and 10 minutes after a standardised bicycle exercise test (duration 15 minutes) in 37 short children (group 1: mean (SD) age 12.8 (3.5) years; mean (SD) bone age 10.4 (3.6) years; mean (SD) height standard deviation score (SDS) -2.8 (0.7], 16 tall children (group 2: mean age 12.9 (2.8) years; mean bone age 13.9 (1.4) years; mean height SDS 3.0 (0.8], and 30 normal children (group 3: mean age 13.3 (3.2) years; mean bone age 12.8 (3.4) years; mean height SDS -0.4 (0.8]. Results of GH are expressed as mean (SEM). The pre-exercise GH was similar in the three groups (group 1, 8.0 (2.3) mU/l, group 2, 8.5 (2.5) mU/l, and group 3, 8.3 (2.3) mU/l). There was a significant rise in GH after exercise in all three groups. GH after exercise was higher in group 2 (35.1 (2.5) mU/l) compared with groups 1 and 3 (17.8 (3.0) and (20.8 (3.2) mU/l). Post-exercise GH was less than 10 mU/l in 29 children (34% total; 49% group 1, 6% group 2, and 34% group 3). There was a positive relation between post-exercise GH and both bone age and public hair stage. Multiple regression analysis revealed that relevant predictors of a rise in GH with exercise were different for the sexes in these children with varying stature: for boys, bone age and pubic hair stage; for girls, height and height SDS. All the tall girls were in puberty. No statistical relation was observed between post-experience GH and cardiovascular response to exercise, time of day of exercise, time of eating before exercise, and plasma insulin or insulin to glucose ratio at time of exercise. We conclude that the GH response to the physiological stimulus of exercise is higher in puberty compared with childhood. Therefore, although children may be suspected of having GH deficiency after a failure of GH to increase after exercise, a non-response may be a normal finding in prepubertal children, independent of stature.
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PMID:Growth hormone response to a standardised exercise test in relation to puberty and stature. 381 36

Growth hormone (GH) responses to growth-hormone-releasing hormone (GRH) and thyrotropin-releasing hormone (TRH) were studied in 17 diabetic patients. Ten patients (group 1) had retinopathy corresponding to stage III-V (Scott's classification), and the remaining seven patients (group 2) had no retinopathy despite longer duration of diabetes in comparison with the patients in group 1. There were no differences in age, percent of ideal body weight, and serum HbA1 levels between the two groups. Basal serum GH levels were 1.9 +/- 0.4 ng/ml (mean +/- SEM) in group 1, and not different from the values in group 2 (1.6 +/- 0.7 ng/ml). However, GH responses to synthetic human GRH-44 (1 micrograms/kg body wt, i.v. bolus) were significantly greater in group 1, as judged by the maximal response or integrated GH secretion after the administration of GRH. There were no differences in serum insulin-like growth factor I (IGF-I) levels between group 1 (262 +/- 35 ng/ml) and group 2 (232 +/- 30 ng/ml), and no significant correlation was found between serum IGF-I levels and GH responses to GRH in either of the two groups. Paradoxical GH responses to TRH (500 micrograms, i.v. bolus) were found in only one patient in each group. We have thus demonstrated that GH responses to GRH are more pronounced in diabetic patients with retinopathy than in patients without this complication, although it remains to be determined whether or not greater GH responses to GRH are causally related to the development of diabetic retinopathy.
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PMID:Growth hormone responses to growth-hormone-releasing hormone and thyrotropin-releasing hormone in diabetic patients with and without retinopathy. 392 95

Elevated plasma concentrations of growth hormone impair glucose tolerance and insulin sensitivity of peripheral tissues. To study the effect of short-term exposure to growth hormone concentrations elevated into the upper physiologic range (7-10 ng/ml) on splanchnic carbohydrate metabolism, both splanchnic glucose output (SGO) and substrate exchange after ingestion of a 75-g glucose load were determined by means of the liver vein catheter technique in six healthy volunteers after growth hormone administration. Growth hormone was infused at a rate of 2 micrograms/kg X h starting 120 min before and continuing for 150 min following the glucose load. Control studies without growth hormone administration were performed in seven subjects. SGO was 104 +/- 10 (SEM) mg/min in the postabsorptive state and increased to 43.4 +/- 2.2 g during the 150-min period following glucose ingestion. Growth hormone infusion did not alter basal SGO (130 +/- 14 mg/min), nor the splanchnic exchange of lactate, pyruvate, and free fatty acids, whereas basal production of beta-OH-butyrate was increased twofold; following glucose ingestion a higher proportion of the given glucose load escaped the splanchnic bed after growth hormone exposure (66.9 +/- 6.8 g/150 min; P less than 0.005). The insulin production rate (basal 14 +/- 2 mU/min; following oral glucose 7.0 +/- 0.8 U/150 min) as calculated from C-peptide release from the splanchnic area was unaltered by growth hormone exposure in the basal state (14 +/- 3 mU/min), but augmented after glucose ingestion (14.8 +/- 1.5 U/150 min).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of growth hormone on splanchnic glucose and substrate metabolism following oral glucose loading in healthy man. 636 Jul 65

Circulating hormone and metabolite profiles have been studied in ten patients with alcoholic cirrhosis, five patients with alcoholic hepatitis and/or fatty liver, and nine normal controls over a 12-h period of meals and activity. Blood glucose was elevated throughout the day in both cirrhotic and non-cirrhotic alcoholics (mean 12-h glucose; controls 5.38 +/- 0.16 (SEM) mmol/l; cirrhotics 6.98 +/- 0.30 mmol/l, P less than 0.001; non-cirrhotics 7.18 +/- 0.26 mmol/l, P less than 0.001). Non-cirrhotic alcoholics had an exaggerated insulin response to meals, whereas cirrhotic patients had hyperinsulinaemia throughout the day (mean 12-h insulin; controls 16.3 +/- 2.3 mU/l; cirrhotics 35.8 +/- 6.6 mU/l, P less than 0.02). Growth hormone levels were elevated only in patients with cirrhosis (mean 12-h growth hormone, 7.06 +/- 1.35 v. 0.85 +/- 0.17 micrograms/l, P less than 0.001). Serum cortisol was persistently elevated in cirrhotics but only in the evening in non-cirrhotic alcoholics. Lactate and pyruvate responses to meals were exaggerated in non-cirrhotic patients whereas in cirrhotics, levels were persistently raised. Blood glycerol was elevated in all alcoholic patients whereas ketone body levels were normal. Hypertriglyceridaemia was observed only in non-cirrhotic patients. No relationship between the endocrine and metabolic state was observed in either cirrhotic or non-cirrhotic patients.
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PMID:Hormone and metabolite profiles in alcoholic liver disease. 641 54

Plasma growth hormone measured at 20-min intervals across the night via indwelling venous cannula revealed a significant reduction in 16 healthy aged men as compared with 14 healthy young men. The decrease in growth hormone was entirely confined to the first 3 hours of the night (M +/- SEM for the integrated level was 5.0 +/- 1.2 and 21 +/- 4.2 ng . hr/ml). Growth hormone across the latter part of the night did not differ. Day and evening growth hormone levels measured hourly in five of the aged and nine of the young men failed to reveal an age effect. Growth hormone release is known to be associated with sleep onset, and particularly with slow wave sleep, stage 3 and 4, which was reduced in amount in these aged men (9.9 +/- 1.9 and 22.8 +/- 2.3% of time in bed for aged and young groups, respectively). Sleep stage 3 and 4 correlated significantly with growth hormone level (R = .463, p less than .01) for young and aged men combined, but not for either age group alone, indicating that growth hormone does not have a direct, simple relationship with slow wave sleep.
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PMID:Plasma growth hormone during sleep in young and aged men. 668 35


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