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)

Twenty-seven patients with symptomatic Paget's disease of bone were randomly treated with mithramycin, glucagon, and calcitonin given either alone or in combination. Mithramycin, at a dose of fifteen micrograms per kilogram of body weight per day, proved to be a relatively safe drug and elicited a rapid response with only transient side effects. Calcitonin combined with mithramycin was the most effective therapy.
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PMID:Combination drug therapy in treatment of Paget's disease of bone: clinical and metabolic response. 14 41

We studied nine consecutive hypocalcemic patients with acute pancreatitis to elucidate the mechanism of hypocalcemia. Mean serum ionized calcium, 0.97 mM, was below the normal mean of 1.16 mM (P less than 0.001). Seven of eight patients tested had normal parathyroid hormone levels. All responded to parenteral parathyroid extract by increasing serum ionized calcium and urinary cyclic AMP, indicating parathyroid-hormone-responsive target organs. Calcitonin and glucagon concentrations were increased above normal in some patients, but there was no relation with serum ionized calcium. Parenteral glucagon had no significant effect on serum ionized calcium or calcitonin concentrations. These findings suggest that neither glucagon nor calcitonin was primarily responsible for the hypocalcemia, which did not produce expected increases in serum parathyroid hormone concentrations. Relative parathyroid insufficiency may account for the persistent hypocalcemia frequently observed in patients with acute pancreatitis.
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PMID:Inadequate parathyroid response in acute pancreatitis. 17 71

Calcitonin gene-related peptide (CGRP) is present in the stomach, and exogenous CGRP stimulates gastric somatostatin release. A study was undertaken to elucidate the functional linkage between CGRP and somatostatin in the stomach. Newborn Wistar rats were made CGRP deficient by intraperitoneal injection of capsaicin 2 days after birth, and then 2.5 mo later, release of CGRP and somatostatin was examined by vascular perfusion of the isolated stomach. In CGRP-deficient rats, neither the content nor basal secretion of gastric somatostatin differed from that in normal rats, and although none of several secretagogues induced CGRP secretion, the somatostatin response to glucagon was well preserved, indicating the presence of normally functioning D cells. On the other hand, arterial infusion of capsaicin significantly increased the release of not only CGRP but also somatostatin from the stomach of normal rats. In CGRP-deficient rats, however, capsaicin produced no corresponding effect. Finally, human CGRP-(8-37), a CGRP-receptor antagonist, completely inhibited the increase of gastric somatostatin induced by both rat alpha-CGRP and capsaicin infusion in normal rats. Thus the capsaicin-induced increase of somatostatin release appears to be mediated by CGRP in the stomach.
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PMID:Linkage between capsaicin-stimulated calcitonin gene-related peptide and somatostatin release in rat stomach. 168 66

To study the influence of the pancreatic neuropeptides, galanin and calcitonin gene-related peptide, on insulin and glucagon secretion in man, synthetic porcine galanin (80 pmol.kg-1.min-1; N = 6) or synthetic human calcitonin gen-related peptide (10 pmol.kg-1.min-1; N = 5) was infused intravenously in human volunteers. Following 5 min of infusion, arginine (5 g bolus + 10 mg.kg-1.min-1) was given. Galanin did not affect basal or arginine-stimulated insulin secretion judged from determinations of plasma insulin and C-peptide. Similarly, galanin did not affect arginine-stimulated glucagon secretion. Calcitonin gene-related peptide did not affect basal or arginine-stimulated insulin or glucagon secretion. However, calcitonin gene-related peptide slightly potentiated the arginine-induced hyperglycemia (p less than 0.01). Thus, in man, galanin has no influence on insulin or glucagon secretion when infused at 80 pmol.kg-1.min-1, whereas CGRP at 10 pmol.kg-1.min-1 induces slight hyperglycemia.
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PMID:Effects of galanin and calcitonin gene-related peptide on insulin and glucagon secretion in man. 170 74

The pharmacological effects of glucagon (0.05 mg/kg b.wt. day) on serum calcium, magnesium and strontium levels were analyzed in order to clarify the response of divalent cations to glucagon administration and its possible relation with calcitonin release stimulation. The results show significant decreases in serum calcium and strontium levels 2 h after glucagon administration, and in daily administration the effect peaks on the 3rd day and returns to baseline values by the 9th day. In contrast, the serum magnesium increases significantly by the 3rd day of daily glucagon administration and continues to increase until the 9th day. Calcitonin administration (90 mU Medical Research Council unit)/100 g b.wt.) significantly reduces the serum calcium, strontium and magnesium levels up to the 3rd day of treatment, just when the glucagon effect is highest. Other additional mechanisms may be involved besides the calcitonin release stimulation, in the response induced in divalent cations--particularly magnesium--by the exogenous administration of glucagon.
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PMID:Effects of glucagon on serum calcium, magnesium and strontium levels in rats. 177 42

Tumor-infiltrating lymphocytes were isolated from a primitive neuroectodermal tumor and fused with GM4672 cells, resulting in hybrids secreting human IgM-kappa antibody, which is reactive to olfactory neuroblastoma tumor cells. Hybridoma clones 4F and 9G produce human monoclonal antibodies reactive to autologous and allogeneic neuroblastoma tumor cells and subsets of pancreatic islet cells in formalin-fixed tissues. They react specifically with dense core granules of glucagon and insulin-producing islet cells, but not with those in cells producing somatostatin. Calcitonin granules are not recognized by these antibodies. The area of localization of the granules is distinct from the component labeled by murine monoclonal antibodies to chromogranin A. The clones have remained stable in culture for over two years and continue to secrete up to 60 micrograms/mL of human IgM. This study demonstrates the possibility of directly analyzing the antibody repertoire of tumor-infiltrating B cells, and this technique may allow the development of human monoclonal antibodies to other novel cellular antigens.
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PMID:Human monoclonal antibodies to neuroendocrine granules derived from tumor-infiltrating lymphocytes isolated from a primitive neuroectodermal tumor. 196 74

Calcitonin gene-related peptide (CGRP) is an intrapancreatic neuropeptide with potential effects on islet hormone secretion. To investigate its pancreatic actions, we examined the effects of a 10 min perfusion of synthetic human CGRP on islet hormone release from the isolated dog pancreas (n = 6) at 5.5 mM glucose. At 0.1 nM, CGRP inhibited insulin secretion (P less than 0.01), which was already observed at 2 min after its introduction. After CGRP perfusion was stopped, a stimulatory off-response occurred. In contrast, at higher dose levels, CGRP stimulated insulin secretion. At 1.0 nM, the stimulation was weak and transient (P less than 0.01), occurring only during the first 3 min of CGRP perfusion. At 10 nM, the stimulation continued for 6 min (P less than 0.05), and at 50 nM, the stimulation was marked and sustained throughout the 10 min perfusion period (P less than 0.01). After the CGRP perfusion at 1.0 and 10 nM, but not at 50 nM, a marked stimulatory off-response in insulin secretion was seen. Glucagon and somatostatin secretion were not significantly affected by CGRP at any of the examined concentrations. We conclude that CGRP exerts dual effects on insulin secretion from the perfused dog pancreas: inhibition at low concentrations and stimulation at high concentrations. This pattern of effect might represent a new regulatory concept for neural influences on islet function: the qualitative response being determined by the amount of neurotransmitter released.
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PMID:Dual effects of calcitonin gene-related peptide on insulin secretion in the perfused dog pancreas. 196 74

Twenty medullary carcinomas of the thyroid gland were examined for the presence of immunoreactive calcitonin, thyroglobulin, glucagon, keratin, gastrin/CCK, carcinoembryonic antibody (CEA), insulin, serotonin, adreno-corticotropic hormone (ACTH), prostatic acid phosphatase, and somatostatin using the immunoperoxidase peroxidase-antiperoxidase technique. In addition, they were stained with mucicarmine, alcian blue/periodic acid-Schiff (PAS), Grimelius, Congo red, crystal violet, and Fontana-Masson stains. Calcitonin-immunoreactive cells were absent in one tumor and present in 19 tumors (95%). Thyroglobulin was present in seven tumors (35%). Twenty tumors contained CEA-immunoreactive cells (100%). Fourteen cases were immunoreactive to serotonin (70%) and 12 were positive for somatostatin (60%). Glucagon- and gastrin/CCK-immunoreactive cells were found in two cases each (10%). Four tumors (20%) contained ACTH-immunoreactive cells and three cases (15%) were positive for prostatic acid phosphatase. Five cases (25%) contained keratin-immunoreactive cells. One case was immunoreactive to insulin (5%). Grimelius-positive cells were present in 19 of the cases (95%). Mucin-containing cells were present in 65% of the cases. The validity of the immunocytochemical localizations was tested by specific absorption of each antibody with the corresponding antigen. The demonstration of immunoreactivity for multiple antigens in each of the 20 cases suggests that the origin of medullary thyroid carcinomas is from a neuroendocrine cell potentially capable of producing numerous hormone substances. In addition, as the neoplastic cells in 35% of the tumors contained hormonal substances as well as thyroglobulin, it is suggested that papillary or follicular tumors mixed with a neuroendocrine component exist more commonly than previously suspected. Finally, psammoma bodies might be present in pure medullary carcinoma of the thyroid gland.
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PMID:Medullary carcinoma of the thyroid gland. Clinical, pathological, and immunohistochemical features with review of the literature. 241 97

After burn trauma, a very marked endocrine response occurs. Almost all the known hormones take part in it. Their response influences very much the postburn metabolic changes and participates in the integration of the body's response with the nervous and immune systems. In this review, mainly the changes in various hormone levels are described, as well as the possible role of the acute phase response after burn trauma, and the communications between the endocrine and immune systems, the cells of the latter are able to respond to various hormonal stimuli and to secrete various hormones themselves. Some of the hormones are very sensitive indicators of the burn stress, e.g., the T3 levels (very low), testosterone in males (very low), dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) (very low), ADH, catecholamines, renin and angiotensin II, cortisol (high), 17-beta-estradiol in males (usually elevated). Other hormones are usually elevated, but not always (ACTH, aldosterone, prolactin, glucagon, immunoreactive insulin, beta-endorphin, rT3, 11-beta-hydroxyandrostenedione), but there are hormones that are unually low (T4, FSH, androstenedione, progesterone--the latter especially in females). Calcitonin, parathyroid hormone, growth hormone are sometimes elevated, as well as LH (measured with RIA methods). TSH is usually normal, the biologically measured LH was reported to be low. The levels of the sensitive indicators of burn stress may be used to evaluate the effect of treatment: if the burn patient is properly treated, the indicators may become earlier normal.
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PMID:Endocrine changes after burn trauma--a review. 251 73

The systemic availability of glucagon and human calcitonin given intranasally to healthy volunteers as spray solutions or powders has been examined. Glucagon was absorbed only when surfactants were used, and 9-lauryl ether (as a spray) and sodium glycocholate (as spray or powder) were equally active. Calcitonin was poorly absorbed when given alone but the surfactants dihydrofusinate (as spray or powder) and glycocholate (as a spray) were equally active in promoting absorption. Thus, enhancers are required to obtain significant nasal absorption of glucagon and calcitonin and powders and spray solutions did not differ in terms of systemic availability.
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PMID:Nasal administration of glucagon and human calcitonin to healthy subjects: a comparison of powders and spray solutions and of different enhancing agents. 259 79


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