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)

1. Using an immunocytochemical procedure a wide range of immunoreactive vertebrate bioactive peptides (BAPs) has been found in hemocytes of Viviparus ater: bombesin, calcitonin, CCK-8, CCK-39, GH, glucagon, insulin, oxytocin, neurotensin, secretin, serotonin, somatostatin, substance P, vasopressin, and VIP. 2. No immunostaining was observed for antigastrin and antithyroglobulin antibodies. 3. The presence of BAP-like molecules in hemocytes suggests a correlation between hemocyte and APUD cells and is evidence of a relationship between the neuroendocrine and the immune systems.
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PMID:The presence of immunoreactive vertebrate bioactive peptide substances in hemocytes of the freshwater snail Viviparus ater (Gastropoda, Prosobranchia). 136 24

Daily hypoxia (6 h, 6000 m) changed the functional state of endocrine pancrease of male and female Wistar rats. The actions of hypoxia on functional state of supraoptic (SO) and paraventricular (PV) nuclei of hypothalamus and islet cells of endocrine pancreas were examined using immunocytochemical, histochemical, morphometric and radioimmunoassay methods. Increase of insulin biosynthesis in beta cells and glucagon secretion of alpha cells, and decrease of the somatostatin contents in delta cells of pancrease islets have been investigated. The functional activity of vasopressinergic magnocellular subnucleus of PV increased, but that of SO decreased with reduction of vasopressin blood concentration at the same time. The functional state of oxytocin synthesis subdivisions of PV and SO were sex dependent, but the oxytocin contents in median eminence increased.
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PMID:[Interactions of the macrocellular neurosecretory system of the hypothalamus and the endocrine pancreas of rats in adaptation to hypoxia]. 136 11

Because of the prominent role of the renal medulla in the elaboration of concentrated urine and the possible differential regulation of the various nephron segments, desensitization to vasopressin (AVP) was studied on freshly isolated rat medullary thick ascending limbs (MTALs) and outer medullary collecting ducts (MCDs). Desensitization was induced through intramuscular injections of 1-deamino-8-D-arginine-vasopressin (dDAVP, 2 micrograms/day for 3 days), the last of which was performed 1 h before kidney removal. The cellular response to AVP was studied by measuring cAMP accumulation in micro-dissected nephron segments. In the MTAL, we observed a marked (around 80%) and selective desensitization to AVP, the response to either glucagon or human calcitonin remaining unaltered. In the MCD, significant desensitization was observed in the presence of 1 nM AVP in the assay medium, and was no longer significant when the AVP concentration was increased to supramaximal levels (10-1,000 nM). These experiments thus reveal a clear dissociation between MTAL and MCD with regards to dDAVP-induced desensitization and extend previous observations made on target segments in the renal cortex.
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PMID:Desensitization to vasopressin action in the rat kidney medulla: studies on isolated nephron segments. 137 64

Sustained production of plasma proteins, notably albumin, is a reliable indicator of the differentiated state of hepatocytes. In this work, we have developed a fetal hepatocyte culture system where studying the regulation of albumin expression in proliferating liver cells. Our results show that under proliferative conditions (i.e., in the presence of EGF) fetal hepatocytes maintain albumin production above control quiescent non-treated cells. Glucagon and noradrenaline have no effect on the proliferation induced by EGF in cultured fetal hepatocytes; however, they act synergistically with the growth factor, increasing intracellular albumin levels. The maximum response is obtained by treatment of cells with EGF and noradrenaline. The stimulatory noradrenergic effect is mimicked by agents that increase cyclic AMP levels (forskolin plus IBMX). However, vasopressin or phorbol esters have no effect on albumin production, neither alone nor in combination with EGF. Dexamethasone, which does not alter the proliferative induction of EGF, increases albumin content. This effect is independent of the proliferative status of the cells and is not enhanced by glucagon, noradrenaline, or cyclic AMP increasing agents. The hormonal changes observed in albumin production partially correlate with changes in mRNA levels. This is the first time that cyclic AMP increasing agents are shown to act synergistically with EGF, increasing the expression of this liver specific gene.
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PMID:Regulation of albumin expression in fetal rat hepatocytes cultured under proliferative conditions: role of epidermal growth factor and hormones. 137

Endocrine abnormalities in patients with chronic renal failure are well documented. The present study aimed to assess the influence of long-term erythropoietin (EPO) therapy on endocrine abnormalities in haemodialyzed patients. Two groups of haemodialyzed patients, each of which comprised 17 subjects, were examined. The first one treated by EPO (EPO group) while the second one did not receive this hormone (NO-EPO group). A complete biochemical and hormonal check-up was performed before and at the 3, 6, 9 and 12 months of the study period. Normal values for the estimated parameters were obtained in appropriately selected sex and age-matched healthy subjects. After EPO therapy an increase of the haematocrit value from 21.8 +/- 0.9% to 32.6 +/- 0.9% was observed which was accompanied by a significant decline of plasma ferritin and saturation of transferrin. In patients of the NO-EPO group a significant although less marked rise of the haematocrit value (21.4 +/- 0.4% to 24.2 +/- 0.6%) was also noticed. EPO therapy did not change electrolytes (Na, K, Ca, inorganic phosphate), osteocalcin, creatinine, glucose and alkaline phosphatase plasma levels as well as plasma concentrations of calcium related hormones (PTH, calcitonin, 1.25(OH)2D3) and vasopressin (AVP). EPO treatment induced a significant decline of somatotropin (HGH), prolactin (PRO), follitropin (FSH), lutropin (LH), ACTH, cortisol, plasma renin activity, aldosterone, insulin (IRI), glucagon (IR-G), pancreatic polypeptide (PP) and gastrin plasma levels and an increase of plasma estradiol, testosterone and atrial natriuretic peptide (ANP). These EPO induced endocrine alterations were restricted mostly to the first 6 months of EPO administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of long-term erythropoietin therapy on endocrine abnormalities in haemodialyzed patients. 145 6

Adenylate cyclase activity was measured on membrane fractions from the gill epithelium of rainbow trout Salmo gairdneri. Basal and glucagon-stimulated activities responded negatively to homologous neurohypophyseal peptides (arginine-vasotocin and isotocin). This inhibitory effect was totally abolished in the presence of pertussis toxin (IAP). The guanine nucleotide dependence of the enzyme was further explored by using GTP, GDP, and their stable analogs Gpp(NH)p, GTP gamma S, and GDP beta S. The results suggest that neurohypophyseal peptides at low concentrations inhibit the adenylate cyclase system directly by way of a Gi-protein, thus implying the intervention of a new type of membrane receptor for these hormones in fish gills.
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PMID:Gi protein mediates adenylate cyclase inhibition by neurohypophyseal hormones in fish gill. 148 May 12

Insulin responsiveness in the human placenta is controversial. This study evaluated insulin stimulation of alpha-aminoisobutyric acid (AIB) uptake in cultured human placental trophoblasts. Both Na(+)-dependent and -independent components of AIB uptake were present in cultured trophoblasts. Na(+)-dependent AIB uptake was significantly stimulated by insulin in a time-dependent manner, as early as 2 h, with a maximum at 12 h of continuous exposure to hormone. Insulin treatment for 4 h increased both the initial uptake rate and the final intracellular concentration. Stimulation was dependent on insulin concentration, with significant stimulation beginning at 10(-9) M. Insulin treatment increased maximum velocity but not the Michaelis constant. Approximately 75% of basal (unstimulated) AIB uptake was inhibited by 10 mM alpha-methylaminoisobutyric acid (MeAIB). The insulin-stimulated increment above basal AIB uptake was completely inhibited by 10 mM MeAIB. Cycloheximide treatment significantly reduced basal and stimulated AIB uptake, although a significant response to insulin persisted. Na(+)-dependent AIB uptake was also stimulated by glucagon, dexamethasone, and 8-bromoadenosine 3',5'-cyclic monophosphate, but not by vasopressin. This study further characterizes amino acid uptake by the human placenta and demonstrates that the Na(+)-dependent component of AIB uptake by the cultured trophoblasts is stimulated by physiological concentrations of insulin.
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PMID:Amino acid transport by the cultured human placental trophoblast: effect of insulin on AIB transport. 156 12

Challenge of intact hepatocytes with one of the hormones vasopressin, angiotensin and glucagon or with the phorbol ester phorbol 12-myristate 13-acetate (PMA) led to a rapid increase in the activity of protein kinase C found in both cytosol and membrane fractions. Maximal activation by hormones occurred within 1-6 min of challenge of cells, after which activity declined. In membrane fractions protein kinase C activity return to basal levels some 15 min after exposure of cells to either angiotensin or glucagon. In cytosol fractions of cells challenged with hormones a second phase of activation ensued after about 10 min, with levels of protein kinase C activity remaining elevated above basal level 15 min afterwards. Activity changes elicited by PMA were rather different; it took about 15 min to achieve maximal activation of cytosolic protein kinase C activity. In membranes of cells challenged with PMA, an initial rapid and transient activation was followed by a sustained increase in activity occurring about 10 min after exposure of cells to this ligand. Only when hepatocytes were challenged with PMA was the translocation of protein kinase C from the cytosol to membrane fraction observed. The kinetics of PMA-induced translocation suggested that it accounted for the second phase of the increase in membrane protein kinase C activity which was unique to this ligand.
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PMID:Glucagon, vasopressin and angiotensin all elicit a rapid, transient increase in hepatocyte protein kinase C activity. 157 78

The effects were investigated of the choleretic bile salt glycoursodeoxycholate (G-UDCA) and of the cholestatic bile salt taurochenodeoxycholate (T-CDCA) on changes in perfusate Ca2+, glucose and oxygen and in bile calcium and bile flow induced by the administration of (a) vasopressin, (b) glucagon and (c) glucagon plus vasopressin together to the perfused rat liver [Hamada, Karjalainen, Setchell, Millard & Bygrave (1992) Biochem. J. 281, 387-392]. G-UDCA itself increased the secretion of calcium in the bile several-fold, but its principal effect was to augment each of the above-mentioned metabolic events except glucose and oxygen output; particularly noteworthy was its ability to augment the 'transients' in bile calcium and bile flow seen immediately after the administration of vasopressin with or without glucagon. T-CDCA, by contrast, produced opposite effects and attenuated all of the parameters measured, and in particular the transients in bile calcium and bile flow. The data provide evidence of a strong correlation between calcium fluxes occurring on both the sinusoidal and the bile-canalicular membranes and that all are modifiable by glucagon, Ca(2+)-mobilizing hormones and bile salts.
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PMID:Acute effects of cholestatic and choleretic bile salts on vasopressin- and glucagon-induced hepato-biliary calcium fluxes in the perfused rat liver. 157

It is well-known that cardiac function in cerebrally dead patients rapidly deteriorates, leaving the organ unfit for donation. This study investigated whether or not cardiac function in patients with cerebral death can be maintained in a desirable condition with hormonal supplementation. In studies of changes in hormones before and after cerebral death, insulin, glucagon, triiodothyronine, thyroxine, cortisol, vasopressin, epinephrine, and norepinephrine values were measured with a lapse of time after cerebral death. Among them, triiodothyronine and cortisol levels were markedly reduced after cerebral death; therefore, these two hormones were selected as hormonal supplements. The average period from the judgment of cerebral death to cardiac arrest was 4.3 days in 12 patients with no hormonal supplement (group I) and more than 11.5 days in 4 patients with hormonal supplement (group II). This period for patients in group II was significantly longer (p less than 0.05). In 2 of the group II patients the hormonal supplementation was discontinued at the family's request, and in the other 2 patients, it was discontinued because of proposed renal donation. Hemodynamic comparisons between the two groups showed that the mean arterial pressure and the left ventricular maximum dp/dt were significantly higher (p less than 0.01) as was the cardiac index (p less than 0.05) on the 3rd day after cerebral death in members of group II. Thereafter, in group II, an excellent hemodynamic state was maintained until hormonal supplements were discontinued. We conclude that the triiodothyronine and cortisol supplements were effective in the maintenance of cardiac function in patients after cerebral death.
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PMID:Effects of hormonal supplements on the maintenance of cardiac function in potential donor patients after cerebral death. 158 Oct 88


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