scholarly journals Tyrosine Hydroxylase Neurons Regulate Growth Hormone Secretion via Short-Loop Negative Feedback

2020 ◽  
Vol 40 (22) ◽  
pp. 4309-4322 ◽  
Author(s):  
Frederick Wasinski ◽  
João A.B. Pedroso ◽  
Willian O. dos Santos ◽  
Isadora C. Furigo ◽  
David Garcia-Galiano ◽  
...  
1995 ◽  
Vol 75 (1) ◽  
pp. 57-61 ◽  
Author(s):  
C. Farmer ◽  
H. Lapierre

Pituitaries from female Yorkshire pig fetuses (90 d, n = 26; 110 d, n = 17) and 6-mo-old pigs (n = 5) were enzymatically dispersed, plated, and cultured for 47 h. The cells were then rinsed and incubated for 22 h with testing media containing 0, 50, 100, 200, 300 or 400 ng mL−1 of IGF-I. Half of the wells from each concentration of IGF-I were then incubated for an additional 3 h with concentrations of IGF-I similar to those in the previous incubation, while the other half also had GRF added to the testing media to reach a final concentration of 10−8 M. Culture media were then collected from all the wells, were frozen, and later assayed for GH. Irrespective of whether GRF was present, IGF-I decreased pituitary secretion of GH (P < 0.001). A significant negative response to IGF-I was already present at the dose of 50 ng mL−1 (P < 0.0001). However, the extent of the GH response to IGF-I seen in pigs of various ages differed depending on whether GRF was present. The present results therefore establish that IGF-I does exert a negative feedback on pituitary GH secretion in swine and that the age-related changes in this feedback are dependent on the presence of GRF. In swine, it appears that high circulating concentrations of GH in late-gestation fetuses are not a result of a lesser sensitivity of the somatotroph to the inhibitory actions of IGF-I. Key words: Pig, cell culture, pituitary, IGF-I, growth hormone, age


2011 ◽  
Vol 301 (4) ◽  
pp. R1143-R1152 ◽  
Author(s):  
Johannes D. Veldhuis ◽  
Cyril Y. Bowers

Although stimulatory (feedforward) and inhibitory (feedback) dynamics jointly control neurohormone secretion, the factors that supervise feedback restraint are poorly understood. To parse the regulation of growth hormone (GH) escape from negative feedback, 25 healthy men and women were studied eight times each during an experimental GH feedback clamp. The clamp comprised combined bolus infusion of GH or saline and continuous stimulation by saline GH-releasing hormone (GHRH), GHRP-2, or both peptides after randomly ordered supplementation with placebo (both sexes) vs. E2 (estrogen; women) and T (testosterone; men). Endpoints were GH pulsatility and entropy (a model-free measure of feedback quenching). Gender determined recovery of pulsatile GH secretion from negative feedback in all four secretagog regimens (0.003 ≤ P ≤ 0.017 for women>men). Peptidyl secretagog controlled the mass, number, and duration of feedback-inhibited GH secretory bursts (each, P < 0.001). E2/T administration potentiated both pulsatile ( P = 0.006) and entropic ( P < 0.001) modes of GH recovery. IGF-I positively predicted the escape of GH secretory burst number and mode ( P = 0.022), whereas body mass index negatively forecast GH secretory burst number and mass ( P = 0.005). The composite of gender, body mass index, E2, IGF-I, and peptidyl secretagog strongly regulates the escape of pulsatile and entropic GH secretion from autonegative feedback. The ensemble factors identified in this preclinical investigation enlarge the dynamic model of GH control in humans.


1986 ◽  
Vol 43 (6) ◽  
pp. 651-656 ◽  
Author(s):  
Mark E. Molitch ◽  
Lucille W. King ◽  
Alan C. Moses ◽  
Sarah Gottesman ◽  
Laura Hlivyak

1976 ◽  
Vol 81 (1) ◽  
pp. 9-18 ◽  
Author(s):  
Paul Saenger ◽  
Ernest Schwartz ◽  
Eckehart Wiedemann ◽  
Lenore S. Levine ◽  
Mary Tsai ◽  
...  

ABSTRACT Baseline somatomedin activity in seven of eight patients with Turner's syndrome was found to be within normal limits. Somatomedin activity readily suppressed with oestrogen administration. The overall mean serum somatomedin activity during oestrogen therapy (0.87 U/ml, sd 0.15) was significantly lower (P < 0.005) than the mean of the control serum somatomedin activities (1.09 U/ml, sd 0.24). During oestrogen therapy, suggestive elevations of fasting growth hormone levels were noted in five of eight patients. The data indicate that oestrogenic suppression of serum somatomedin was not due to decreased growth hormone secretion and suggest the existence of a negative feedback link between somatomedin and growth hormone.


1990 ◽  
Vol 126 (2) ◽  
pp. 237-244 ◽  
Author(s):  
R. W. Lea ◽  
C. A. Ahene ◽  
J. A. Marsh ◽  
S. Harvey

ABSTRACT The i.c.v. administration of 0·1 or 10 μg ovine (o)GH to 12- to 16-week-old hypothyroid chickens of a sex-linked dwarf (SLD) strain suppressed the basal plasma GH concentrations, measured 24 h afterwards. The GH response of the oGH-injected SLDs to TRH was suppressed, in a dose-related way, in comparison with that induced by TRH in birds given control injections (10 μg) of bovine serum albumin (BSA). Basal circulating concentrations of GH in euthyroid K strain birds of the same age were even lower than in the SLDs following injection of 10 μg oGH, and were not further reduced by oGH administration. The GH response to TRH in the K strain birds injected i.c.v. with 0·1 or 10 μg oGH was, nevertheless, suppressed in comparison with the BSA-injected K strain controls. The i.c.v. administration of oGH also suppressed circulating concentrations of LH and the LH response to TRH in the K strain birds. Twenty-four hours after i.c.v. administration of oGH (10 μg), the somatostatin (SRIF) content in the medial basal hypothalamus of 8-week-old euthyroid cockerels was greater than that in BSA (10 μg)-injected controls. At the same time, the binding of [3H]3-methyl-histidine2-TRH to the pituitary caudal and cephalic lobes of GH-injected birds was less than that in the controls. These results suggest that GH regulation in avian species is partly mediated by an inhibitory short-loop mechanism (mediated by hypothalamic SRIF and a down-regulation of pituitary TRH-binding sites) that suppresses basal and secretagogue-induced GH release. Journal of Endocrinology (1990) 126, 237–244


1983 ◽  
Vol 56 (3) ◽  
pp. 486-488 ◽  
Author(s):  
WALLACE B. MENDELSON ◽  
LAURENCE S. JACOBS ◽  
J. CHRISTIAN GILLIN

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