Physiological Role of Somatostatin in Regulation of Pulsatile Growth Hormone Secretion

Tannenbaum, Gloria Shaffer

doi:10.1007/978-1-4615-7886-4_14

Cited by 34 publications

(10 citation statements)

References 100 publications

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“…We have demonstrated that the normal ultradian GH rhythm is virtually obliterated in response to food deprivation, insulinopenic diabetes, and intracellular glucopenia [7], Passive immunization with anti-somatostatin serum restored high-amplitude GH secretory bursts in both starved and diabetic rats, which suggests that circulating somatostatin plays a physiological role in mediating the GH suppression ob served in these conditions.…”

Section: Somatostatin As a Mediator Of Disorders Of Gh Secretionmentioning

confidence: 88%

Somatostatin as a Physiological Regulator of Pulsatile Growth Hormone Secretion

Tannenbaum

1988

Horm Res

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Somatostatin plays an important role in the regulation of the episodic and ultradian rhythm of growth hormone (GH) secretion. Passive immunization of rats with specific antibodies to the 14 and 28 amino acid sequences caused a significant GH elevation. The fact that somatostatin antiserum was unable to block episodic GH surges indicates that this hormone’s release must be regulated by a dual mechanism. Indeed, GH-releasing factor (GRF) seems to be instrumental in the maintenance of pulsatile GH secretion. Moreover, exogenous GRF induced a further GH increase predominantly during the period of active secretion. Neutralization of endogenous somatostatin eliminated this time-dependent effect, indicating that this peptide blocks periodical spontaneous GH release. Food deprivation and changes in glucose homeostasis virtually obliterate the ultradian GH rhythm. In this context, peripheral somatostatin seems to play an important role. Also the central GRF/somatostatin interplay is responsible for a short-loop feedback control on pituitary somatotrops.

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Section: Somatostatin As a Mediator Of Disorders Of Gh Secretionmentioning

confidence: 88%

Somatostatin as a Physiological Regulator of Pulsatile Growth Hormone Secretion

Tannenbaum

1988

Horm Res

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“…Within the brain, SRIF acts as a neuromodulator with widespread physiological effects on neuroendocrine, cognitive, and behavioral f unctions (Tannenbaum, 1985;Epelbaum et al, 1994). Accordingly, deficits in SRIF and SRI F receptors have been documented in a number of neurological disorders, including epilepsy (Schwarzer et al, 1996) and Alzheimer's disease (Epelbaum et al, 1994).…”

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confidence: 99%

Interrelationships between Somatostatin sst2A Receptors and Somatostatin-Containing Axons in Rat Brain: Evidence for Regulation of Cell Surface Receptors by Endogenous Somatostatin

Dournaud

Boudin²,

Schönbrunn³

et al. 1998

J. Neurosci.

114

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Using an antipeptide antibody, we reported previously on the distribution of the somatostatin sst2A receptor subtype in rat brain. Depending on the region, immunolabeled receptors were either confined to neuronal perikarya and dendrites or distributed diffusely in tissue. To investigate the functional significance of these distribution patterns, we examined the regional and cellular relationships between somatostatin axons and sst2A receptors in the rat CNS, using double-labeling immunocytochemistry. Light and confocal microscopy revealed a significant correlation ( p Ͻ 0.02) between the distribution of somatodendritic sst2A receptor immunoreactivity and that of somatostatin terminal fields, both quantitatively and qualitatively. Furthermore, in regions of somatodendritic labeling, a subpopulation of sst2A-immunoreactive cells was also immunopositive for somatostatin, suggesting that a subset of sst2A receptors consists of autoreceptors. By contrast, in regions displaying diffuse sst2A labeling only moderate to low densities of somatostatin terminals were observed, and no significant relationship was found between terminal density and receptor immunoreactivity.At the electron microscopic level, areas expressing somatodendritic sst2A labeling were found by immunogold cytochemistry to display low proportions of membrane-associated, as compared with intracellular, receptors. Conversely, in regions displaying diffuse sst2A receptor labeling, receptors were predominantly associated with neuronal plasma membranes, a finding consistent with the high density of sst2 binding sites previously visualized in these areas by autoradiography. Double-labeling studies demonstrated that in the former but not in the latter regions, sst2A-immunoreactive somata and dendrites were heavily contacted by somatostatin axon terminals. Taken together, these results suggest that the low incidence of membrane-associated receptors observed in regions of somatodendritic sst2A labeling may be caused by downregulation of cell surface receptors by endogenous somatostatin, possibly through ligand-induced receptor internalization.

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“…G R F stimulates G H secretion, whereas SRIF inhibits it [1]. Considerable evi dence suggests that G H regulates its own secretion through hypothalamic G R F and SRIF.…”

Section: Introductionmentioning

confidence: 99%

Negative Regulation of Hypothalamic Growth Hormone-Releasing Factor Messenger Ribonucleic Acid by Growth Hormone and Insulin-Like Growth Factor I

Uchiyama

Kaji²,

Abe³

et al. 1994

Neuroendocrinology

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Increased growth hormone-releasing factor messenger ribonucleic acid (GRF mRNA) and decreased somatostatin (SRIF) mRNA levels have been reported in the hypothalamus of hypophysectomized rats as well as of dwarf mice. In order to elucidate the effect of the growth hormone-insulin-like growth factor I (GH-IGF-I) axis on hypothalamic GRF and SRIF synthesis, we measured levels of mRNA coding for GRF and SRIF and for pituitary GH in pubertal male rats treated for 3 weeks with antirat GRF γ-globulin (GRF-ab), anti-SRIF γ-globulin (SRIF-ab) or both. Immunoneutralization of circulating endogenous GRF resulted in a marked decrease in serum IGF-I and pituitary GH mRNA levels in Northern blot analysis, whereas it caused a significant increase in GRF mRNA levels in the arcuate nucleus as assessed by both Northern blot and in situ hybridization analysis. SRIF mRNA levels in the periventricular nucleus were slightly decreased by GRF-ab treatment when analyzed by in situ hybridization, but not significantly after Northern blot analysis. Immunoneutralization of circulating endogenous SRIF failed to affect mRNA levels of hypothalamic GRF and SRIF but caused a slight reduction in pituitary GH mRNA levels. Levels of mRNA coding for hypothalamic GRF and pituitary GH were also measured by Northern blot analysis in young male rats treated with rat GRF-ab for 2 weeks and replaced with rat GH or IGF-I for the second 1 week. Replacement with either rat GH or IGF-I suppressed the increased hypothalamic GRF mRNA levels. These data indicate that endogenous GRF is essential for normal synthesis of pituitary GH and that both GH and IGF-I negatively regulate the synthesis of hypothalamic GRF.

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Physiological Role of Somatostatin in Regulation of Pulsatile Growth Hormone Secretion

Cited by 34 publications

References 100 publications

Somatostatin as a Physiological Regulator of Pulsatile Growth Hormone Secretion

Somatostatin as a Physiological Regulator of Pulsatile Growth Hormone Secretion

Interrelationships between Somatostatin sst2A Receptors and Somatostatin-Containing Axons in Rat Brain: Evidence for Regulation of Cell Surface Receptors by Endogenous Somatostatin

Negative Regulation of Hypothalamic Growth Hormone-Releasing Factor Messenger Ribonucleic Acid by Growth Hormone and Insulin-Like Growth Factor I

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