Physiological Role of Growth Hormone (GH)-Releasing Factor and Somatostatin in the Dynamics of GH Secretion in Adult Male Rat

Sato, Makoto; Takahara, Jiro; FUJIOKA, Yuzuru; Niimi, Michio; Irino, Shozo

doi:10.1210/endo-123-4-1928

Cited by 35 publications

(17 citation statements)

References 29 publications

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“…The pulsatile secretion of GH is regulated by the reciprocal interplay of hypothalamic GHRH and somatostatin (32)(33)(34)(35) and by responsivity of the somatotrope cells to these regulatory peptides (28). In general, the amount of GHRH released at any given level of somatostatin tone determines the amount of GH released per secretory episode, and the pattern of somatostatin action determines the frequency and duration of the GH secretory bursts (36)(37)(38).…”

Section: Discussionmentioning

confidence: 99%

Deconvolution Analysis of Spontaneous Nocturnal Growth Hormone Secretion in Prepubertal Children with Preterminal Chronic Renal Failure and with End-Stage Renal Disease

et al. 1995

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We sought to determine whether elevated circulating growth hormone (GH) concentrations in uremic prepubertal children are due to an increase in GH secretory activity by the pituitary gland or a decrease in the metabolic clearance of GH consequent to reduced GFR. Deconvolution analysis was applied to the nighttime plasma GH profiles of 1 ) 11 children with preterminal chronic renal failure, 2) 12 children with end-stage renal disease (ESRD), and 3) a control group of matched children with idiopathic short stature (n = 12). Mean (t SEM) half-life of endogenous GH in children with ESRD (27.5 ? 2.7 min) and preterminal chronic renal failure (23.1 ? 2.1 min) was significantly higher than in controls (14.8 ? 1.6 min; p < 0.001). GH half-life correlated inversely with GFR (r = -0.65, p < 0.001).The number of GH secretory bursts110 h in ESRD (8.1 ? 0.4) was amplified compared with preterminal chronic renal failure (6.4 2 0.5) and with controls (5.9 ? 0.4; p < 0.005). GH production rate varied over a broad range in the three groups: It was highest in ESRD (202 ? 56.6 mg/L/10 h; range 36-683), mainly as a result of an increased number of GH secretory bursts, and not statistically different in preterminal chronic renal failure (66.2 ? 11.4 mg/L/lO h; range 25-168) and in controls (129 ? 27.7 mg/L/10 h; range 39-392). Increased GH half-life, in concert with an increased GH production in some individuals with ESRD, leads to a 2.5-fold increase in the mean plasma GH concentration in ESRD compared with the two other groups ( p < 0.005). However, total immunoreactive plasma IGF-I levels were indistinguishable between groups. This disruption of the normal relationship between circulating GH and total plasma IGF-I levels in ESRD suggests a relative insensitivity to the action of GH in uremia, at least in those target organs (e.g. liver) that contribute predominantly to circulating IGF-I levels. regulation of the frequency and amplitude of pulsatile GH secretion, cannot be quantitated accurately in single blood determinations. Measurements of pulsatile plasma GH concentrations have been performed in prepubertal (4) and pubertal (5) children with CRF. Unfortunately, both studies lacked suitable control groups and did not provide insights into neurosecretory events and concurrent hormone clearance that together underlie the plasma GH pulse patterns. Such information is important particularly in patients with CRF, because the kidney is believed to account for a substantial fraction of the total plasma turnover of GH in humans (25-53%) (6) and in rats (67%) (7). Thus, in children with CRF, the question remains unresolved whether increased plasma GH concentrations are primarily due to increased GH secretion or decreased GH elimination by the kidney.

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Section: Discussionmentioning

confidence: 99%

Deconvolution Analysis of Spontaneous Nocturnal Growth Hormone Secretion in Prepubertal Children with Preterminal Chronic Renal Failure and with End-Stage Renal Disease

et al. 1995

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“…It is unlikely that this attenuation of the G H response can be attributed to remnant endogenous SRIF secretion, because Arsenijeric et al (30) have reported that transient desenstization to repeated G R F pulses was observed in rats which were passively immunized against SRIF. In addition, we have found that desensitization to multiple G R F pulses can be observed even in a rat anterior pituitary perifusion system in which the effect of SRIF is excluded (10). Therefore, it is thought that the diminishing response to repeated G R F injections found in the present study was attributable to either depletion of the releasable intracellular G H pool or to impairment of the G R F receptor such as by downregulation (31).…”

Section: Discussionmentioning

confidence: 45%

“…Recently, there has been much interest in the hypothalamic interactions between G R F and SRIF (8, 9), but the pituitary interactions between these two peptides occurring during G H secretion still remain unclear. We previously investigated the dynamic relationship between G R F and SRIF in the regulation of pulsatile GH secretion in a perifusion system using cultured rat anterior pituitary cells (10). Our data suggested that prolonged pre-exposure to SRIF could prevent an attenuated response to repeated GRF pulses, and that co-exposure to continuous SRIF with brief pauses and hourly GRF pulses could produce large GH surges.…”

mentioning

confidence: 85%

Effects of Somatostatin on the Growth Hormone‐Releasing Factor‐Induced Growth Hormone Secretion in Rats with Electrical and Chemical Inhibitions of Endogenous Growth Hormone‐Releasing Factor and Somatostatin

Sato

Takahara

Niimi

et al. 1990

J Neuroendocrinology

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The episodic pattern of growth hormone (GH) secretion of the male rat was simulated in rats exhibiting impaired GH-releasing factor (GRF) and somatostatin (SRIF) secretion, by administering various combinations of human GRF-(1-44)NH2 (hGRF) and SRIF. Electrical lesions of the arcuate nucleus resulted in a marked decrease in the amplitude of GH secretory bursts, while the administration of cysteamine (200 mglkg) did not change the GH secretory profile in rats with arcuate nucleus lesions. lmmunohistochemical examinations revealed a marked decrease of GRF and SRlF immunoreactivity in the median eminence of the cysteamine-treated rats with arcuate nucleus lesions. The intravenous injection of 5 pg of hGRF every 3 h caused equivalent surges of GH in the cysteamine-treated rats with arcuate nucleus lesions. The additional infusion of 4 pglh of SRlF during the trough periods of GH secretion did not affect the amplitude of the GH surges. Hourly injection of 5 pg of hGRF caused transient desensitization to hGRF. Interestingly, the additional infusion of 4 pglh of SRlF every 3 h enhanced the amplitude of the GH bursts induced by the fourth and the seventh hGRF injections. However, the more frequent injection of 5 pg of hGRF every 30 min caused constant desensitization to hGRF with time, and the additional infusion of 4 pglh of SRlF every 3 h did not change the attenuated responses to hGRF. These results indicated that the simultaneous administration of hourly GRF and continuous SRlF with brief pauses was most effective for producing high GH peaks. This simulation model suggests that SRlF may play an important role not only in the production of GH troughs, but also in the maintenance of GH surges with distinct peaks in the male rat.

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“…Considerable evidence indicates that T3 stimulates the GH gene transcription and subsequently increases GH secretion [1][2][3]. Although it is also established that pulsatile GH secretion is mediated by hypothalamic GRH and somatostatin secretion [15][16][17], the stimulatory action of thyroid hormone on GH secretion occurs at the pituitary level rather than at the hypothalamic level [18,19]. Serum IGF-I levels were not significantly different from normal in hyperthyroid patients despite the increase in urinary GH.…”

Section: Discussionmentioning

confidence: 99%

Relationship between Thyroid Functions and Urinary Growth Hormone Secretion in Patients with Hyper- and Hypothyroidism.

et al. 1994

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Abstract.Thyroid hormone plays an important role in growth hormone (GH) synthesis and secretion. To study the relationship between thyroid function and urinary GH secretion in the hyperthyroid and hypothyroid states, we measured thyroid hormones, simultaneously with serum and urinary GH levels, in 54 patients with thyroid diseases.GH-releasing hormone (GRH) test was performed in 18 patients in order to evaluate serum and urinary GH responses to GRH in hyper-and hypothyroid states. Serum thyroid hormone levels were strongly correlated with the urinary GH levels in the patients, and the correlation was greater than that between serum thyroid hormone and serum GH levels. Urinary GH levels were significantly higher in the hyperthyroid patients than in the euthyroid and hypothyroid patients, although serum GH levels were not significantly different among these three groups. Serum GH response to GRH was significantly decreased in hyperthyroid patients as compared to euthyroid patients. However, urinary GH levels after GRH administration were not decreased in the hyperthyroid patients.These results suggest that hyperthyroid states increase GH in urine and may accelerate the urinary clearance of GH.

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Physiological Role of Growth Hormone (GH)-Releasing Factor and Somatostatin in the Dynamics of GH Secretion in Adult Male Rat

Cited by 35 publications

References 29 publications

Deconvolution Analysis of Spontaneous Nocturnal Growth Hormone Secretion in Prepubertal Children with Preterminal Chronic Renal Failure and with End-Stage Renal Disease

Deconvolution Analysis of Spontaneous Nocturnal Growth Hormone Secretion in Prepubertal Children with Preterminal Chronic Renal Failure and with End-Stage Renal Disease

Effects of Somatostatin on the Growth Hormone‐Releasing Factor‐Induced Growth Hormone Secretion in Rats with Electrical and Chemical Inhibitions of Endogenous Growth Hormone‐Releasing Factor and Somatostatin

Relationship between Thyroid Functions and Urinary Growth Hormone Secretion in Patients with Hyper- and Hypothyroidism.

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