Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The insulinotropic effects of alpha-ketoisocaproic acid and glucose reveal many common characteristics in vivo and in vitro. They qualify as initiators of insulin release, their action is amplified by potentiators of insulin release, and they have a similar potency at equimolar concentrations. The dynamics of insulin release evoked by alpha-ketoisocaproic acid and glucose are similar. Epinephrine completely inhibits the insulinotropic effect of glucose and alpha-ketoisocaproic acid. Mannoheptulose exhibits a complete, immediate and reversible blockade of glucose-induced insulin release. In contrast, inhibition of alpha-ketoisocaproic acid-induced insulin release occurs after a lag period and is not reversed by removal of the inhibitor. alpha-ketoisocaproic acid, at equimolar concentrations, is several-fold more effective than glucose in elevating cAMP content in islet. alpha ketoisocaproic acid and glucose are about equally effective in stimulating somatostatin release from isolated rat pancreatic islets. This stimulation is inhibited by epinephrine. Mannoheptulose inhibits only somatostatin release induced by glucose but not by alpha-ketoisocaproic acid. It suggested that the insulinotropic characteristics of glucose and alpha-ketoisocaproic acid reveal many common features, while their mode of action appears to be different.
Mol Cell Endocrinol 1978 Jun
PMID:Comparison of alpha-ketoisocaproic acid and glucose in rats: effects on insulin and somatostatin release and on islet cAMP content. 21 60

Thus far, somatostatin has been used primarily as a research tool to investigate pancreatic alpha- and beta- cell function. On the basis of its ability to inhibit insulin and glucagon secretion, several therapeutic applications have been suggested: e.g., as an adjunct in the treatment of diabetes mellitus, or as a palliative agent in inoperable islet tumors. Current experiments are underway to develop more specific analogs with longer durations of action to permit clinical evaluation of these potential applications. The presence of somatostatin within the pancreatic D cells raises the possibility that it may function as a local regulator of insulin and glucagon release. Clearly, further work is needed to delineate the factors governing the secretion of somatostatin and its mode of action. Such studies may uncover a new class of syndromes resulting from D-cell dysfunction.
Curr Top Mol Endocrinol 1976
PMID:Somatostatin and the endocrine pancreas. 21 Oct 5

The mechanisms of enzymic inactivation of thyrotropin-releasing hormone, luteinizing hormone-releasing hormone and somatostatin, the three fully-characterized hypothalamic regulatory hormones, and the possible physiological significance of the peptidases in neuroendocrine control has been reviewed. Application of the criteria of enzyme location (at the sites of biosynthesis, release, action, elimination and excretion), appropriate biochemical characteristics of the enzymes and changes in enzyme activity in physiological circumstances all suggest that the peptidases can contribute to the mechanisms controlling the hypothalamic hormones' release and actions. Besides their physiological function, the enzymes may also be directly involved in certain pathological conditions. There is evidence to indicate that the enzymes degrading the regulatory hormones may participate in the process of hormone activation as well as inactivation. A continuing investigation of the peptidases may lead to a better understanding of the established endocrine and other putative functions of these hypothalamic polypeptide hormones.
Mol Cell Endocrinol 1979 Apr
PMID:Mechanisms of inactivation of hypothalamic regulatory hormones. 22 39

Substance P stimulation of salivation in rats has been studied as has its in vitro enhancement of amylase release by isolated parotid cells. The extent of the stimulation on amylase release by isolated parotid cells was dependent upon the concentration of substance P, with the minimum effective concentration being 1 nM. The substance P effect was detectable within 1 min after incubation and lasted for at least 50 min. Substance P stimulation was demonstrable at 25--37 degrees C but not at 0 degrees C. Adrenocorticotropic hormone (ACTH), thyrotropin-releasing hormone (TRH), vasopressin and neurotensin had no effect on amylase release. These results suggest that substance P may act directly on the parotid cells. Examination of the salivary-stimulating activity of fragments of substance P showed that the C-terminal octapeptide and (pyroglutamyl)hexapeptide were active, although less potent than substance P, whereas its free acid, C-terminal tetra- and tri-peptides were inactive. Vasopressin, angiotensin II and neurotensin could inhibit substance P induced salivation, whereas TRH, ACTH and somatostatin had no effect. Amylase activity per unit volume of saliva was not changed by the injection of vasopressin, angiotensin II or neurotensin. These vasoactive peptides did not affect substance P stimulation of amylase release by isolated parotid cells. The results indicate that vasopressin, angiotensin II and neurotensin inhibit the action of substance P on salivation at sites other than the parotid cells.
Mol Cell Endocrinol 1979 Sep
PMID:Substance P stimulation of amylase release by isolated parotid cells and inhibition of substance P induction of salivation by vasoactive peptides. 22 41

Two minutes after the intravenous administration of 1 ml of sheep somatostatin antiserum in the rat, plasma growth hormone (GH) levels had reached a maximal 10-15-fold increase which remained approximately constant up to 90 min. The injection of sodium pentobarbital (2 mg/100 g body wt) led to a rapid and transient rise of plasma GH levels of similar magnitude (10-fold) reached 20 to 40 min after injection of the narcotic. The important finding is, however, that the combined administration of somatostatin antiserum and pentobarbital or morphine led to an almost exact additive effect on the plasma GH concentrations. These data, beside providing additional evidence for the existence of GH-releasing activity (GH-RH), indicate that morphine and pentobarbital stimulate GH secretion through increased release of GH-RH.
Mol Cell Endocrinol 1977 Feb
PMID:Stimulated release of hypothalamic growth hormone-releasing activity by morphine and pentobarbital. 32 63

In order to study the control of vasopressin-release, the effect of a series of potential agents was studied in an in vitro perifusion system of rat neurohypophysis after in vivo treatment with nialamide, a monoamine oxidase inhibitor. In this system, metlatonin stimulated vasopressin-release in a dose-dependent manner (1 x 10-8 to 1 x 10-3 M). Serotonin (1 x 10-3 M) also led to a significant increase of vasopressin-release whereas quipazine (1 x 10-3 M), a putative serotonin agonist and monoamine oxidase inhibitor, caused a 3-fold stimulation of the release of the neurohormone. The stimulatory effects of melatonin and serotonin were prevented by omission of Ca2+ combined to an excess of Mg2+ (12mM) in the perifusion medium. 1 x 10-6 M somatostatin did not affect basal or melatonin-stimulated vasopressin-release. These results show that melatonin and serotonin can have a direct stimulatory effect on vasopressin release at the neurohypophyseal level.
Mol Cell Endocrinol 1979 May
PMID:Melatonin-and serotonin-stimulated release of vasopressin from rat neurohypophysis in vitro. 46 80

Increasing the extracellular K+ concentration to 71 mM causes a phasic release of growth hormone and efflux of 45Ca from perifused bovine pituitary cells. Verapamil (20 micron) partially inhibits the initial phase of growth hormone release and 45Ca efflux and completely inhibits the second phase. Somatostatin (1 microgram/ml) partially inhibits both phases of growth hormone release but does not modify 5+-induced 45Ca efflux. Incubation of pituitary cells in 71 mM K+ increases 45Ca incorporation; verapamil (20 micron) completely prevents, and somatostatin (1 microgram/ml) partially inhibits, the K+-induced increase in 45Ca incorporation. The results suggest that 71 mM K+ increases both calcium entry into the cells and calcium redistribution within them, and that verapamil only inhibits the K+-induced calcium entry. Somatostatin may inhibit calcium entry into tissue stores.
Mol Cell Endocrinol 1978 Jan
PMID:Effects of somatostatin and verapamil on growth hormone release and 45Ca fluxes. 62 36

Administration of sodium thiamylal (50 mg/kg,i.p.) and morphine (3 mg/animal,s.c.) leads to high plasma levels of growth hormone (GH) with a maximum measured approximately 30 min after injection. When the same dose of morphine is administered 60 and 120 min later and small additional doses of thiamylal are injected to maintain the animals deeply anesthetized, constant high levels of plasma GH are maintained up to the last interval studied (3 h). This in vivo model has been used to evaluate the potency and duration of action of somatostatin and of six of its analogs by serial blood sampling of animals bearing a cannula inserted into the right superior vena cava. A significant inhibitory effect of somatostatin (45% inhibition) is observed 15 min after a s.c. injection of 1 mug of the peptide while a near maximal effect (90-95% inhibition) is found at a dose of 25 mug. Both the degree of inhibition and duration of action of somatostatin are dose-dependent. Inhibitory activities equivalent to 1-250 mug of somatostatin can be measured with the model described. [Tyr1] somatostatin, [D-Ala1]somatostatin, [N-acetyl-Cys3] somatostatin and [N-benzoyl-Cys3] somatostatin have activities indistinguishable from somatostatin itself while [D-Lys4] somatostatin and [des-amino1, des-carboxy14] somatostatin have approximately 10% the activity of the natural hypothalamic peptide. This in vivo model offers advantageous characteristics of precision and reproducibility for the evaluation of potency of inhibitors of GH release.
Mol Cell Endocrinol 1976 Jan
PMID:Inhibition by six somatostatin analogs of plasma growth hormone levels stimulated by thiamylal and morphine in the rat. 124 67

Using an immunohistochemical technique involving unlabeled antibody and the peroxidase-anti-peroxidase complex, we have localized somatostatin (or growth hormone-release inhibiting hormone), a hypothalamic hormone which can also inhibit gastrin secretion, in the rat stomach. Somatostatin was found to be present in a few cells in the mucosa of the pyloric antrum. These cells are characterized by the presence of secretory granules of about 150-250 nm in diameter and are probably endocrine cells.
Mol Cell Endocrinol 1976 Mar
PMID:Immunohistochemical localization of somatostatin in endocrine cells of the rat stomach. 126 32

Immunocytochemical localization of 5-hydroxytryptamine (5-HT) in the nervous system and aggregate tissue cultures was performed employing an antibody to 6-OH-1,2,3,4-tetrahydro-beta-carboline. A number of immunochemical and biochemical tests with the antigen and the antibody and some procedural changes in the methodology applied for immunolocalization revealed the anti-5-HT-like affinity of the antibody, if applied in paraformaldehyde-fixed tissues. Studies in the hypothalamus, striatum, brainstem, spinal cord, and pineal gland show the complexities of the serotoninergic system. Ultrastructural immunocytochemistry with the preembedding technique reveals that 5-HT synapses are of the asymmetric type. The presynaptic element contains clear, round, small vesicles, with some large dense-core vesicles. The contacts are made with the somata and primary, secondary dendrites or with spines of non-5-HT neurons. Presynaptic dendrites are found in the n. raphe dorsalis, contacting non-5-HT dendrites. Double immunocytochemical methods demonstrated contacts of 5-HT fibers on enkephalin containing neurons of the spinal trigeminal nucleus and on somatostatin containing neurons of the medullary reticular formation. In vitro studies of cultured mesencephalic neurons were performed with the method of aggregating cultures. Such development of a miniature organized nerve tissue was followed up to 35 d in culture. Organization of the neuropil and synaptogenesis was studied using standard electron microscopy. The differentiation of neurons and astrocytes was studied using antibodies to 5-HT and GFAP. Serotonin immunoreactivity could be observed in neuronal bodies and processes at light microscope level as early as the fourth day of culture.(ABSTRACT TRUNCATED AT 250 WORDS)
Mol Neurobiol 1992
PMID:Antibodies as molecular probes in neurobiology. Identification of chemically defined neurons and synapses in tissues and tissue cultures. 128 32


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