Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The endocrine glands of the human foetus are active early in gestation, and various foetal and placental hormonal contributions are essential for growth and sexual differentiation. 1. The anterior pituitary gland has the ability to synthesize, store and secrete hormones early in gestation. The patterns of change in plasma concentrations of hGH (Fig. 1), ACTH, LH and FSH (Fig. 2) during gestation indicate that secretion is at a maximum at mid-gestation, followed by a progressive decrease towards term. The high levels at mid-gestation can be interpreted as due simultaneously to a high secretion rate, low peripheral catabolism and absence of feedback mechanism. In contrast, the secretions of PRL (Fig. 1) and TSH are moderate at mid-gestation and only increase in the last trimester of gestation. 2. Effective control by the central nervous system (CNS) of the pituitary secretions is still immature at mid-gestation. The presence in the foetal hypothalamus of releasing factors such as LRF (Fig. 5) and TRF, and of somatostatin (Fig. 6), a growth hormone release inhibiting factor (GIF), has been established. TRF and GIF, but not LRF, are also present in the cerebral cortex. It has been postulated that, early in life, relatively autonomous and unrestrained secretion of hypothalamic hypophysiotropic releasing factors occurs, and that, later in development, there is a maturation of inhibitory or restraining influences mediated via the CNS (feedback mechanisms) that modulates the secretion of the foetal adenohypophyseal hormones (Fig. 3 and 4). 3. Observations made with anencephalic newborn confirm that a functional hypothalamus is necessary during foetal life for the secretion of each of the hormones of the anterior pituitary gland with the exception of PRL, the secretion of which is normal in anencephaly. Although somatostatin probably participates in the regulation of hGH during foetal life, it appears evident from the anencephaly data that this regulation can only be fully understood by postulating the existence of a growth hormone releasing factor (GRF).
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PMID:[Ontogenesis of hypothalamic control of adenohypophyseal secretions in the human foetus (author's transl)]. 11 47

The anterior pituitary gland of the human fetus has the ability of synthetizing, storing and secreting hormones early during gestation. The patterns of plasma concentrations of hGH, ACTH, LH and FSH during gestation indicate a maximum of secretion at mid-gestation followed by a progressive decrease of these concentrations until term. In contrast, the secretions of PRL and TSH are moderate at mid-gestation and only increase in the last trimester of gestation. Effective control by the central nervous system (CNS) of the pituitary secretions is still immature at mid-gestation. The presence of releasing factors in the fetal hypothalamus has been established (TRF, LRF, somatostatine) and it was postulated that early in life, relatively autonomous and unrestrained secretion of hypothalamic hypophysiotropic releasing factors occurs and, later in development, there was a maturation of inhibitory or restraining influences mediated via the CNS that modulate the secretion of the fetal adenohypophyseal hormones. Observations made with anencephalic newborns confirm that a functional hypothalamus is necessary for the secretions of each of the hormones of the anterior pituitary gland with the exceptiion of PRL, the secretion of which is normal in anencephaly. Although somatostatin probably participates in the regulation of hGH during fetal life, it appears evident that this regulation can only be fully understood with the existence of a GRF (Growth Hormone Releasing Factor).
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PMID:[Hypothalamic factors in the human fetal brain: their role in the ontogeny of fetal hypophyseal functions]. 20 94

Intravenous (i.v.) administration of TRF (1 mg/kg) increases the LD50 of pentobarbital (PB) by 25% while the same dose of somatostatin results in a 30% reduction in PB LD50. A similar increase of PB LD50 by TRF was observed in hypophysectomized rats. Mortality was completely abolished in rats receiving TRF (1 mg/kg) ten minutes after a lethal dose of PB (120 mg/kg). Somatostatin (1 mg/kg) decreases strychnine-induced seizure duration and increases strychnine LD50 by 21% while TRF lowers the strychnine LD50 by 28%. These observations are consistent with central nervous system sites of action for TRF and somatostatin.
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PMID:Central nervous system effects of hypothalamic peptides. 80

Radioimmunoassays of brain extracts have shown that several peptides occur in high concentrations in the CNS. The releasing-factor peptides TRF, LRF, somatostatin, CRF and GRF have the highest concentration in the hypothalamic extracts. High levels of somatostatin, CCK octapeptide, neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP) are found in cortical extracts. Substance P, CCK, NPY, and enkephalins are present in high concentrations in basal ganglia and mesolimbic areas. Pharmacological doses of these peptides result in several behavioural and vegetative effects. Immunocytochemical studies show that the CNS peptides are localised in neurones and in synaptic vesicles. In vitro studies with brain tissues show that peptides are capable of modifying the ongoing classical neurotransmission. In depressive patients several neuropeptides (CCK, CRF and NPY) have been shown to have low CSF levels. Patients dying of senile dementia have low cortical levels of somatostatin, CRF and substance P. In schizophrenic patients CCK peptides have shown to improve some symptoms. At present the therapeutic potentials of peptides are poorly known. More studies are required to understand their role in neurotransmission and related pathological states.
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PMID:Peptides and neurotransmission in the central nervous system. 282 29

Several neural peptides have been demonstrated to influence central nervous system control of nutrient metabolism. The principal mechanism by which these peptides influence peripheral nutrient metabolism is by altering the secretion of adrenal epinephrine. Bombesin or its mammalian counterpart, gastrin releasing peptide, and TRF act within the brain to stimulate the secretion of epinephrine from the adrenal gland. Associated with these changes in epinephrine secretion is a reduction of plasma insulin and elevation of plasma glucagon and glucose. Somatostatin and various somatostatin analogs act in the brain to inhibit adrenal epinephrine secretion stimulation by a variety of stimuli.
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PMID:Neuropeptides: central nervous system effects on nutrient metabolism. 611 88

Corticotropin-releasing factor (CRF) injected into the brains of rats produces hyperglycemia and an increase in plasma concentrations of glucagon, epinephrine, and norepinephrine. Neither hypophysectomy nor adrenalectomy prevents CRF-induced hyperglycemia. However, a role of adrenal epinephrine release in mediating CRF-induced hyperglycemia is supported by the finding that the central nervous system-selective somatostatin analog, desAA1,2,4,5,12,13-[D-Trp8]somatostatin, totally prevents the elevation of plasma epinephrine and suppresses the rise of plasma glucose but does not alter the increase in plasma norepinephrine induced by CRF. Pretreatment with the ganglionic blocker chlorisondamine completely prevents the CRF-induced rises in plasma glucose, epinephrine, and norepinephrine. These results demonstrate that CRF acts within the brain to stimulate sympathetic outflow, which results in the development of hyperglycemia. In contrast to other peptides that act within the central nervous system, e.g. bombesin, TRF, and beta-endorphin, whose hyperglycemic actions depend exclusively on adrenal epinephrine secretion, CRF-induced hyperglycemia is secondary to the enhanced secretion of both epinephrine and norepinephrine.
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PMID:Corticotropin-releasing factor: actions on the sympathetic nervous system and metabolism. 704 76

Experiments with primary cultures demonstrated a stimulating effect of TRF on somatotropic hormone (STH) secretion by hypophyseocytes of neonatal but not adult rats and a reduced reactivity of neonatal somatotrophs to the inhibitory effect of somatostatin during short-term incubation. No noticeable serotonin effect on STH release from hypophyseal cells of animals of various ages was observed. During prolonged (24 h) incubation a weak inhibitory effect of bromocriptine and melatonin on STH secretion by pituitary cells of neonatal but not adult rats was observed. These results permit us propose a similarity of the functional characteristics of neonatal pituitary somatotrophs to somatomammotroph properties.
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PMID:[Age-related features of neurohumoral regulation of somatotropic hormone secretion]. 791 Sep 60

Several neural peptides have been demonstrated to influence central nervous system control of nutrient metabolism. The principal mechanism by which these peptides influence peripheral nutrient metabolism is by altering the secretion of adrenal epinephrine. Bombesin or its mammalian counterpart, gastrin releasing peptide, and TRF act within the brain to stimulate the secretion of epinephrine from the adrenal gland. Associated with these changes in epinephrine secretion is a reduction of plasma insulin and elevation of plasma glucagon and glucose. Somatostatin and various somatostatin analogs act in the brain to inhibit adrenal epinephrine secretion stimulation by a variety of stimuli.
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PMID:Neuropeptides: Central nervous system effects on nutrient metabolism. 2794 15