Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Central injection of thyrotropin-releasing hormone (TRH) potently blocked the development of, as well as rapidly reversed, 2-deoxyglucose (2-DG)-stimulated hyperglycemia in mice. The antihyperglycemic effect was dose-related, dependent upon the structural integrity of the peptide, dissociated from the peptide's hypophysiotropic action and from its interaction with TRH receptors, and mediated by the cholinergic parasympathetic system. Moreover, TRH blocked the rise in plasma glucose following central injection of corticotropin-releasing factor, enkephalin, clonidine and glucagon, as well as the hyperglycemic response to immobilization, electric foot shock or endotoxin administration. These results indicate that TRH, acting within the central nervous system, can block neurally-mediated hyperglycemia in addition to its previously reported actions to elicit systemic hypoglycemia in normoglycemic mice and to antagonize epinephrine-stimulated hyperglycemia in these animals.
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PMID:Thyrotropin-releasing hormone blocks neurally-mediated hyperglycemia through central action. 289 45

Neuropeptides and biogenic amines known to be present in neurons or afferent terminals in the paraventricular nucleus (PVH), supraoptic nucleus (SON) and/or lateral hypothalamus (LH) were added to small areas of these structures obtained by micropuncture and cyclic adenosine monophosphate (cAMP) levels were measured. cAMP accumulation occurred in PVH, SON and LH in response to neuropeptides of the secretin family, such as vasoactive intestinal peptide (VIP) and in response to catecholamines. Bradykinin, alpha-melanocyte-stimulating (alpha-MSH), luteinizing hormone-releasing hormone (LH-RH), oxytocin and carbamylcholine stimulated cAMP accumulation selectively in one or two of the above structures. Glucagon, cholecystokinin (CCK), somatostatin (SRIF), corticotropin-releasing factor (CRF), thyrotropin-releasing hormone (TRH), adrenocorticotropin (ACTH), melanocyte-stimulating hormone (MSH), methionine enkephalin (Met-Enk), beta-endorphin, neurotensin, bombesin and angiotensin II did not effect cAMP levels while leucine enkephalin (Leu-Enk), arginine vasopressin and gamma-aminobutyric acid (GABA) elicited regionally selective decreases in basal levels of cAMP. When interactions between some of these compounds were measured, VIP and norepinephrine exerted a more than additive effect on cAMP elevation in the PVH, while the effect on cAMP of the SON and LH was additive.
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PMID:Interaction of neuropeptides and biogenic amines on cyclic adenosine monophosphate accumulation in hypothalamic nuclei. 300 57

We studied 14 alcoholic men without evidence of liver damage. After two weeks of alcohol abstinence, the patients were divided into two groups of seven patients each. Hypothalamic-hypophysial, thyroid, and gonadal axis tests were done on group 1 patients before disulfiram administration, and the tests were later repeated while the patients were taking disulfiram. Group 2 patients had initial testing done while taking disulfiram and repeat testing after the drug was stopped. The following abnormalities were found and were not affected by disulfiram: lack of suppression of both growth hormone and glucagon with oral glucose intake, and lack of response of follicle-stimulating hormone after administration of synthetic gonadotropin-releasing hormone. After disulfiram administration, we noticed a blunted response of thyrotropin to thyrotropin-releasing hormone.
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PMID:Evaluation of the hypothalamic-hypophysial, thyroid, and gonadal axes before and after disulfiram administration in patients with chronic alcoholism. 305 25

Based on the fact that human pancreas has thyrotropin-releasing hormone (TRH) immunoreactivity and bioactivity, we studied the effect of TRH on peripheral plasma levels of pancreatic glucagon (IRG) and insulin (IRI) in healthy subjects. During the infusion of 400 micrograms TRH for 120 min basal plasma IRI and IRG levels did not change significantly. In addition, intravenous infusion of 400 micrograms TRH did not affect the increments in the plasma IRG levels and the decrements in the blood glucose during insulin hypoglycemia.
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PMID:Lack of effect of thyrotropin-releasing hormone (TRH) on the peripheral plasma levels of pancreatic glucagon in man. 308

Histidyl-proline diketopiperazine (His-Pro DKP) cells in the pancreas of human fetuses aged between 12 and 19 wk were localized by the indirect antibody-enzyme method on semithin sections. To study their fine structure, two techniques were used: a superimposition technique consisting of comparison of the same cells in semithin and electron microscopic preparations, and an immunocytochemical technique on ultrathin sections using the unlabeled antibody peroxidase-antiperoxidase method. Our results show that (a) the same cells are positive for both His-Pro DKP and glucagon/glicentin, (b) His-Pro DKP immunoreactive cells possess extremely electron-opaque secretory granules, implying that these cells correspond to the A cells, and (c) His-Pro DKP immunoreactivity is found over the secretory granules. We hypothesize that the two peptides His-Pro DKP and thyrotropin-releasing hormone (TRH) have independent origins, since TRH is found in the B cells.
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PMID:Histidyl-proline diketopiperazine (His-Pro DKP) immunoreactivity is present in the glucagon-containing cells of the human fetal pancreas. 310 58

Injections of 10 micrograms/kg thyrotropin-releasing hormone (TRH) 150 microliter intracisternally (i.c.) in conscious rabbits evoked behavioral excitation and compulsive scratching, tachypnoea, an increase of heart rate and blood pressure, oxygen consumption and hyperthermia. TRH i.c. significantly increased free thyroid hormone and calcitonin secretion during depressed thyrotropin (TSH) secretion. The rise of calcitonin correlated with a fall of serum calcium. The ergotropic function of TRH i.c. was further demonstrated by rapid increases of glucagon, serum glucose, free fatty acid and free glycerol, with a delayed rise of insulin depending on glucose levels. The increases of free thyroid hormones, calcitonin, cortisol and lipolysis following TRH i.c. were augmented after spinal transection, while glucagon secretion increased at a slower rate, however, not accompanied by rises of glucose and insulin. Behavioral excitation and lipolysis were augmented by TRH i.c. after total thyroidal denervation, which completely prevented the rise in thyroid hormone and calcitonin secretion, although the thyroid follicles and C cells responded properly to TSH. Section of all thyroidal nerves except the recurrent laryngeal nerve reduced mainly calcitonin secretion following TRH i.c., while the behavioral, autonomic and other endocrine responses were augmented. Additional abdominal vagotomy in these rabbits diminished glucagon secretion by about 50% without significantly changing the other effector responses. Taking 125I-labelled TRH concentration in the cerebrospinal fluid at the site of i.c. injection as 100%, then 58% of TRH penetrated into outer parts of the dorsal and ventral medulla oblongata and pons, and 8% into the neuropil of the aqueductal region. Radioactivity in other brain areas including the hypothalamus was below 1%, while the hypophysis was practically devoid of radiolabelled TRH. It is suggested that the observed behavioral, autonomic and endocrine activity pattern elicited by injection of TRH into the cisterna magna was caused by excitation of neurons confined to that compartment and was mediated by pathways of the reticular formation of the lower brainstem, with the concept that TRH-containing neurons are intrinsic excitatory constituents of the 'activating reticular system'.
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PMID:Selective autonomic nervous control of thyroid hormone and calcitonin secretion during metabolic and cardiorespiratory activation by intracisternal thyrotropin-releasing hormone (TRH). 314 96

An assay for the binding of [(3)H]thyrotropin-releasing hormone ([(3)H]TRH) is described. Plasma membranes isolated from bovine anterior pituitary gland bind about 600 femtomoles of this hormone per mg of protein, as compared to 15 femtomoles per mg of protein in the total adenohypophyseal homogenate (40-fold purification). The equilibrium constant of membrane receptor-[(3)H]TRH binding at 0 degrees C is 4.3 x 10(7) L.M(-1), or a half-maximal binding of this hormone at 23 nM. The binding is time-dependent; addition of unlabeled hormone induces dissociation of the receptor-[(3)H]TRH complex with a half-life of 14 min. The binding of TRH is not altered by 10 muM melanocyte-stimulating hormone-release inhibiting hormone, lysine-vasopressin, adrenocorticotropin, growth hormone, prolactin, luteinizing hormone, insulin, glucagon, L-thyroxine, or L-triiodothyronine. K(+) and Mg(++) increase formation of the receptor-TRH complex at optimal concentrations of 5-25 mM and 0.5-2.5 mM, respectively, with inhibition at higher concentrations. Ca(++) inhibits binding of TRH at all concentrations tested.
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PMID:Binding of thyrotropin-releasing hormone to plasma membranes of bovine anterior pituitary gland (hormone receptor-adenylate cyclase-equilibrium constant-( 3 H)thyrotropin). 462 48

It is now clear that a variety of neuropeptides interact with the more classically defined neurotransmitters to stimulate or inhibit feeding. An extensive peripheral peptide satiety system has been identified. Peptides involved in this system include cholecystokinin, bombesin, gastrin-releasing peptide, glucagon, somatostatin, and possibly thyrotropin-releasing hormone and calcitonin. Some of these peptides appear to inhibit feeding by activating ascending fibers in the vagus, whereas others exert their actions independent of the vagus. In addition, neuropeptides appear to play a role in producing the neuromodulatory effects of taste on appetite, and hormones from the endocrine system modulate neuropeptide effects on feeding. The central appetite regulatory system appears to be arranged in a cascade, with an interaction between dynorphin and dopamine producing a part of the feeding drive. This drive is held in check by a variety of neuropeptides including calcitonin, corticotropin-releasing factor, and bombesin. In turn, these peptides are modulated by a norepinephrine-alpha-aminobutyric acid (GABA) system. Neurotensin, serotonin, cyclohistidyl proline diketopiperazine, and the peripheral satiety system appear to modulate the norepinephrine-GABA disinhibitory system. By the judicious use of neuropharmacological modeling we have developed a model of the neurotransmitter interactions involved in appetite regulation that can act as a springboard for the design of future experiments to unravel the mysteries of appetite regulation.
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PMID:Neuropeptides and appetite: contribution of neuropharmacological modeling. 614 55

The effects of vasoactive intestinal peptide (VIP) and several other peptides have been examined on cyclic AMP accumulation in intact pieces and isolated horizontal cells of the teleost (carp) retina. VIP was the most effective peptide examined, inducing a dose-related response, and an approximately fivefold increase in cyclic AMP production when used at a concentration of 10 microM. Porcine histidine isoleucine-containing peptide and secretin, peptides structurally related to VIP, also stimulated cyclic AMP accumulation, but at concentrations of 10 microM induced responses which were only approximately 40% and 10%, respectively, of the response observed with 10 microM VIP. In contrast, several other peptides, including glucagon, neurotensin, somatostatin, luteinizing hormone-releasing hormone, alpha-melanocyte-stimulating hormone, cholecystokinin octapeptide26-33, gastrin-releasing peptide, thyrotropin-releasing hormone, and VIP10-28 were totally inactive. The response to 10 microM VIP was not antagonized by several dopamine antagonists, indicating the presence of a population of specific VIP receptors coupled to adenylate cyclase, distinct from the population of dopamine receptors coupled to adenylate cyclase also known to be present in this tissue. Finally, experiments involving the use of fractions of isolated horizontal cells indicate that these neurons possess a population of VIP receptors coupled to cyclic AMP production which would appear to share a common pool of adenylate cyclase with a population of similarly coupled dopamine receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of vasoactive intestinal peptide and other peptides on cyclic AMP accumulation in intact pieces and isolated horizontal cells of the teleost retina. 619 61

The brain contains a large variety and number of peptides some of which were known earlier as hypothalamic hormones (vasopressin, oxytocin, luteinizing hormone-releasing hormone, thyrotropin-releasing hormone, somatostatin) or as pituitary hormones (the family of opiomelanocortins), while others, not primarily known as hypothalamic or pituitary hormones, may also have endocrine effects (substance P, angiotensin II, neurotensin, bombesin, vasoactive intestinal peptide (VIP), gastrin-cholecystokinin, glucagon, carnosine, bradykinin). These peptides, which form a new class of putative neurotransmitters, are present early in brain development and show important sex differences in both their pattern of innervation and their effects. Their peripheral effects may include intrauterine growth of the placenta and fetus, the timing of birth, acceleration of the course of labour and responses to haemorrhage (redistribution of cardiac output and stimulation of blood cell formation). Endogenous peptides are probably involved in brain development, which may explain their general, permanent and sex-dependent effects when given in the period of rapid brain development. Although peptides might in the future be useful for stimulating recovery from retarded brain development, at present one should be aware of the potential dangers of their use in, for example, obstetrics.
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PMID:Development of peptidergic systems in the rat brain. 627 64


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