The Effects of Phenothiazines on Endocrine Function: II

1974 ◽  
Vol 124 (582) ◽  
pp. 420-430 ◽  
Author(s):  
P. J. V. Beumont ◽  
C. S. Corker ◽  
H. G. Friesen ◽  
T. Kolakowska ◽  
B. M. Mandelbrote ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Rhesus Monkey ◽  
Sex Hormones ◽  
Human Subjects ◽  
Endocrine Function ◽  
Ample Evidence ◽  
Experimental Animals ◽  
High Doses

There is ample evidence that high doses of phenothiazines and other neuroleptics depress the pituitary-gonadal axis in experimental animals (De Wied, 1967), but the effects of these drugs on sex hormones in human subjects are still controversial (Shader and Di Mascio, 1970). Literature concerning growth hormone (GH) is even more controversial, since phenothiazines have been found to inhibit GH release in rodents (Muller et al., 1967) but to increase it in the rhesus monkey (Meyer and Knobil, 1967). In human subjects phenothiazines have been reported to depress both basal levels of GH and the response to hypoglycaemia (Sherman et al., 1971), while others have found that this response is enhanced (Schimmelbusch, Mueller and Scheps, 1971). Studies of prolactin levels are more consistent, showing raised prolactin both in experimental animals and in human subjects following administration of phenothiazines (Apostolakis et al., 1972; Hwang et al., 1971; Kleinberg et al., 1971; Sulman, 1970).

Graded cryohypophysectomy in the rhesus monkey

1972 ◽  
Vol 36 (2) ◽  
pp. 169-177 ◽  
Author(s):  
Suleyman Saglam ◽  
Clifford L. Kragt ◽  
Charles B. Wilson ◽  
Selna L. Kaplan ◽  
Marvin Barker
Keyword(s):  
Growth Hormone ◽  
Rhesus Monkey ◽  
Pituitary Gland ◽  
Rhesus Monkeys ◽  
Endocrine Function ◽  
Posterior Lobe ◽  
Content Type ◽  
Predetermined Time ◽  
Fine Print ◽  
Damaging Effects

✓ Histopathology and endocrine function of the pituitary gland of rhesus monkeys subjected to graded cryohypophysectomy were compared with the histopathology and endocrine function in hypophysectomized and sham-operated monkeys. Freezing at −50°, −100°, and −150°C destroyed 72.3%, 78.3%, and 93.1% of the pituitary respectively. The posterior lobe was more resistant to the damaging effects of cold. A nearly complete (96.3%) histological hypophysectomy was accomplished at −190°C; nearly all remaining viable tissue was in the posterior lobe. Freezing at −150°C appears to result in a complete functional hypophysectomy. Of the adenohypophyseal cells, the gonadotropin-secreting cells were the most susceptible to cold, with the growth-hormone-producing cells next in susceptibility. Adrenocorticotropin-secreting cells were more resistant. Cells producing thyroid-stimulating hormones were not susceptible, and the pituitary stalk was quite resistant to the damaging effects of freezing at these temperatures. Thus, a predictable partial hypophysectomy by means of cryosurgery seems feasible, and, with a predetermined time, it is evident that the degree of cold is critical in achieving a complete cryohypophysectomy.

SEX HORMONES – EFFECTS ON PROLACTIN CELLS IN THE RAT, DOG, MONKEY AND MAN

1974 ◽  
Vol 77 (3_Supplb) ◽  
pp. S3-S15 ◽  
Author(s):  
M. F. El Etreby ◽  
P. Günzel ◽  
G. Soulioti
Keyword(s):  
Sex Hormones ◽  
Anterior Pituitary ◽  
Morphological Changes ◽  
Prolactin Secretion ◽  
Prolactin Cells ◽  
Experimental Animals ◽  
Exogenous Application ◽  
Endogenous Production ◽  
High Doses

ABSTRACT Histomorphological and immunocytochemical methods were used to study the effect of either physiological and pathological endogenous production or long-term exogenous application of high doses of sex (steroid) hormones on the prolactin cells in the anterior pituitary of experimental animals and man. Using these methods it was shown that enhanced endogenous secretion of sex hormones, mainly of oestrogens, seems to produce nearly the same morphological changes in the anterior pituitary of the rat, dog and man. It was also possible to show that long term exogenous application of high doses of oestrogens or oestrogens and progestagens can stimulate prolactin cells in some experimental animals. The demonstration of similar mechanisms in man calls for more extensive investigations on the possible role of the sex hormones on prolactin secretion.

Growth hormone signaling and action in obese versus lean human subjects: evidence of increased hepatic GH sensitivity in obesity

2017 ◽  
Author(s):  
Morten Hogild Pedersen ◽  
Ann Mosegaard Bak ◽  
Steen Bonlokke Pedersen ◽  
Niels Jessen ◽  
Niels Moller ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Human Subjects ◽  
Hormone Signaling

METABOLIC EFFECTS OF “PITUITARY GROWTH HORMONE PREPARATIONS” IN HUMAN SUBJECTS SUMMARY OF QUANTITATIVE STUDIES EXTENDING OVER A FIVE-YEAR PERIOD

1954 ◽  
Vol 14 (1) ◽  
pp. 110-117 ◽  
Author(s):  
LAURANCE W. KINSELL ◽  
SHELDON MARGEN ◽  
JOHN W. PARTRIDGE ◽  
GEORGE D. MICHAELS ◽  
HARRY E. BALCH ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Human Subjects ◽  
Metabolic Effects ◽  
Pituitary Growth Hormone ◽  
Quantitative Studies

scholarly journals Growth hormone signaling and action in obese versus lean human subjects

2019 ◽  
Vol 316 (2) ◽  
pp. E333-E344 ◽  
Author(s):  
Morten Lyng Høgild ◽  
Ann Mosegaard Bak ◽  
Steen Bønløkke Pedersen ◽  
Jørgen Rungby ◽  
Jan Frystyk ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Growth Hormone ◽  
Human Subjects ◽  
Glucose Production ◽  
Relative Increase ◽  
Antagonistic Effect ◽  
Endogenous Glucose Production ◽  
Metabolic Adaptation ◽  
Igf I

Growth hormone (GH) levels are blunted in obesity, but it is not known whether this relates to altered GH sensitivity and whether this influences the metabolic adaptation to fasting. Therefore, we investigated the effect of obesity on GH signal transduction and fasting-induced changes in GH action. Nine obese (BMI 35.7 kg/m2) and nine lean (BMI 21.5 kg/m2) men were studied in a randomized crossover design with 1) an intravenous GH bolus, 2) an intravenous saline bolus, and 3) 72 h of fasting. Insulin sensitivity (hyperinsulinemic, euglycemic clamp) and substrate metabolism (glucose tracer and indirect calorimetry) were measured in studies 1 and 2. In vivo GH signaling was assessed in muscle and fat biopsies. GH pharmacokinetics did not differ between obese and lean subjects, but endogenous GH levels were reduced in obesity. GH signaling (STAT5b phosphorylation and CISH mRNA transcription), and GH action (induction of lipolysis and peripheral insulin resistance) were similar in the two groups, but a GH-induced insulin antagonistic effect on endogenous glucose production only occurred in the obese. Fasting-induced IGF-I reduction was completely abrogated in obese subjects despite a comparable relative increase in GH levels (ΔIGF-I: lean, −66 ± 10 vs. obese, 27 ± 16 µg/l; P < 0.01; ΔGH: lean, 647 ± 280 vs. obese, 544 ± 220%; P = 0.76]. We conclude that 1) GH signaling is normal in obesity, 2) in the obese state, the preservation of IGF-I with fasting and the augmented GH-induced central insulin resistance indicate increased hepatic GH sensitivity, 3) blunted GH levels in obesity may protect against insulin resistance without compromising IGF-I status.

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