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

Eight insulin-dependent non pregnant (IDD-NP), 10 insulin-dependent pregnant (IDD-P) and 9 pregnant control women were studied. During intravenous arginine challenge (ATT) there were lower glucose and higher glucagon plasma levels in the IDD-P when compared to the IDD-NP. IRG levels in response to ATT were also significantly higher in diabetic than in non diabetic control pregnant women. These results seem to indicate that pregnancy in diabetic women, in contrast to that observed in normal women, enhances glucagon secretion with impairment of the physiological mechanism of the facilitated anabolism present in normal pregnancy.
 ...
PMID:Influence of pregnancy on glucagon levels in insulin-dependent diabetic women. 39 52

Urinary (CPU) and plasma C peptide values at baseline (CP0) and under stimulation with glucagon were determined in healthy subjects (n = 17) and in insulin-dependent (IDD, n = 45) and non insulin-dependent (NIDD, n = 32) diabetics. A significant difference in the parameters of insulin secretion (x? SD) was found on the one hand between the IDD group (CPU = 5.58 +/- 5.58 nmol/24 h; CP = 0.14 +/- 0.08 nmol/l; maximum C peptide value after stimulation (CPmax) = 0.33 +/- 0.31 nmol/l; C peptide delta (delta CP) = 0.14 +/- 0.14 nmol/l; area under the curve (A) = 5.00 +/- 4.84) and the NIDD group (CPU = 15.47 +/- 8.22 nmol/24 h; CP = 0.64 +/- 0.28 nmol/l; CPmax = 1.14 +/- 0.44 nmol/l; delta CP = 0.50 +/- 0.31 nmol/l; A = 17.5 +/- 5.86) and on the other hand between the IDD group and the control group (CPU = 18.20 +/- 8.40 nmol/24 h; CP = 0.41 +/- 0.11 nmol/l; CPmax = 1.00 +/- 0.31 nmol/l; delta CP = 0.69 +/- 0.20 nmol/l; A = 17.10 +/- 4.45). As regards the NIDD group, only the fasting C peptide and delta C peptide values were significantly different from those found in the control group. The significance of each parameter of insulin secretion was also studied. There was a correlation between the values of C peptidaemia before and after stimulation with glucagon. However, the correlation between plasma C peptide and urinary C peptide values was mediocre, probably because of the numerous variability factors which intervene in the urinary excretion of C peptide.
 ...
PMID:[C-peptide assays of the urine and plasma at baseline and under stimulation with glucagon in healthy subjects and diabetics]. 214 Jan 81

The glomerulopressin activity of the ultrafiltrate obtained from the peripheral blood of normal subjects, newly diagnosed Type I (insulin-dependent) diabetic patients (IDD), and in normal subjects treated with glucagon was studied in two bioassays: tonic tension contraction of the rat stomach fundus (TTC) and increase in the ureteral pressure of the toad, which was considered as a glomerular pressure index (delta GPI). The ultrafiltrate of four normal volunteers had a low activity in the TTC assay, and in two subjects no activity was observed. The ultrafiltrate of five of these subjects had no activity in delta GPI. In IDD patients the ultrafiltrates were active in the TTC assay and in the toad assay. In glucagon treated normal volunteers three of the ultrafiltrates were very active in the TTC assay and other three had a low activity. In the toad assay five of them were active and no response was observed in one subject. These observations suggest that glomerulopressin activity is increased in peripheral venous blood of untreated newly diagnosed IDD patients and in normal subjects treated with glucagon.
 ...
PMID:Glomerulopressin activity in peripheral blood of newly diagnosed type I (insulin-dependent) diabetic patients and in normal subjects treated with glucagon. 311 Nov 73

In order to better understand the role of A- and B-cell function in diabetic pregnancy, we studied four groups of pregnant women at week 34-36 of gestation. Seventeen were healthy controls (C), 24 had gestational diabetes (GD), 16 had type 2 diabetes (NIDD) and 37 had type 1 diabetes (IDD). At times -20, 0, 20, 30, 45, 60, 90 and 120 min from the beginning of a 30 min infusion of 30 g of arginine intravenously, plasma glucose, glucagon (IRG) and C-peptide (CPR) were measured. Plasma glucose was higher in diabetic than in control subjects. IRG values were also higher in the GD and the NIDD women. CPR values were similar to, or slightly higher than control values in the GD and the NIDD and were much lower in the IDD women. All three variables increased during the arginine infusion in all groups, with the exception that CPR remained unchanged in the IDD. The CPR/IRG molar ratio was similar in control, GD and NIDD women; in the IDD, it was much smaller than in the other groups and was not affected by arginine. In all the diabetic patients, IRG was negatively correlated with the maternal weight gain and in the IDD IRG was positively correlated with the increase in the insulin need and with the CPR levels. In conclusion diabetes appeared to enhance the A-cell function also in pregnancy, possibly impairing the 'facilitated anabolism' and stressing the 'accelerated starvation' which are typical of normal pregnancy. Glucagon was confirmed as one possible determinant of the insulin resistance seen in diabetic pregnancy.
 ...
PMID:Endocrine pancreatic function in insulin-dependent diabetic pregnant women. 353 67

Insulin-induced hypoglycemias are a sign of non-sufficient counterregulation, in which different contra-insulinary hormones participate. The aim of the study was to investigate, whether there exists a difference between IDD and non-diabetics regarding secretion of glucagon, cortisol, and growth hormone during an insulin-induced hypoglycemia and further on pointing out, expecially, the importance of glucagon. Insulin-induced hypoglycemias are counterregulated in non-diabetics, not in IDD. The missing glucagon secretion during insulin-induced hypoglycemia in IDD seems to be independent from an autonomic neuropathy. Only after high doses of exogenous glucagon can one see a counterregulating increase of glucose. The STH secretion is similar in non-diabetics and IDD during an insulin-induced hypoglycemia and has evidently only a secondary effect in hypoglycemic counterregulation. The STH secretion may be the expression of a diencephal-triggered stress situation. The cortisol secretion is the same in both groups. The gluconeogenetic effect of cortisol is not sufficient to accomplish a fast compensation of hypoglycemia. This does not exclude long-term effects. When inhibiting the secretion of insulin and different contra-insulinary hormones with somatostatin, one is able to demonstrate that glucagon alone is a sufficiently counterregulatory hormone in insulin-induced hypoglycemias.
 ...
PMID:[Glucagon, growth hormone, and cortisol response to insulin-induced hypoglycemia in insulin-dependent diabetics (IDD) without autonomic neuropathy (author's transl)]. 700 32

Gateways to Clinical Trials is a guide to the most recent clinical trials in current literature and congresses. The data in the following tables has been retrieved from the Clinical Studies Knowledge Area of Prous Science Integrity, the drug discovery and development portal, http://integrity.prous.com. This issue focuses on the following selection of drugs: Abetimus sodium, adalimumab, alefacept, alemtuzumab, almotriptan, AMGN-0007, anakinra, anti-CTLA-4 Mab, L-arginine hydrochloride, arzoxifene hydrochloride, astemizole, atazanavir sulfate, atlizumab; Belimumab, BG-9928, binodenoson, bosentan, botulinum toxin type B, bovine lactoferrin, BufferGel; Caspofungin acetate, ciclesonide,cilomilast, ciluprevir, clofarabine, CVT-3146; Darbepoetin alfa, desloratadine, diflomotecan, doripenem, dronedarone hydrochloride, drotrecogin alfa (activated), DT388-GM-CSF, duloxetine hydrochloride, E-5564, efalizumab, enfuvirtide, esomeprazole magnesium, estradiol acetate, ETC-642, exenatide, exisulind, ezetimib; Febuxostat; Gallium maltolate, ganirelix acetate, garenoxacin mesilate, gefitinib; H11, HuMax; IL-15, IDD-1, IGIV-C, imatinib mesylate, ISIS-14803, ITF-1697, ivabradine hydrochloride; KRN-5500; L-365260, levetiracetam, levosimendan, licofelone, linezolid, LJP-1082, lopinavir lumiracoxib; MCC-478, melatonin, morphine hydrochloride, morphine-6-glucuronide, moxidectin; N-Acetylcarnosine, natalizumab, NM-702, NNC-05-1869, NSC-703940; Ocinaplon OM-89, omalizumab, omeprazole/ sodium bicarbonate, OPC-28326, ospemifene; PEG-filgrastim peginterferon alfa-2a, pegsunercept, pirfenidone, pralmorelin, pregabalin; Recombinant glucagon-like peptide-1 (7-36) amide, repifermin, RSD-1235; S-8184, selodenoson, sodium dichloroacetate, suberanilohydroxamic acid; TAS-102, terfenadine, teriparatide, tipranavir troxacitabine; Ximelagatran; YM-337.
 ...
PMID:Gateways to clinical trials. 1473 33

Gateways to Clinical Trials is a guide to the most recent clinical trials in current literature and congresses. The data in the following tables has been retrieved from the Clinical Studies Knowledge Area of Prous Science Integrity, the drug discovery and development portal, http://integrity.prous.com. This issue focuses on the following selection of drugs: Abetimus sodium, Ad5-FGF4, adeno-Interferon gamma, AE-941, AERx, alemtuzumab, alicaforsen sodium, almotriptan, alpharadin, anakinra, anatumomab mafenatox, ANG-453, anti-CTLA-4 Mab, AP-12009, aprepitant, aripiprazole, arsenic trioxide, astemizole, atlizumab, atomoxetine hydrochloride; Bevacizumab, BG-9928, BMS-188667, botulinum toxin type B, BufferGel; Caffeine, CDP-870, cetuximab, cilomilast, ciluprevir, clofarabine, continuous erythropoiesis receptor activator, CP-461; Darbepoetin alfa, deferasirox, desloratadine, desoxyepothilone B, diflomotecan, dolasetron, drotrecogin alfa (activated), duloxetine hydrochloride; ED-71, efalizumab, efaproxiral sodium, EKB-569, eletriptan, EMD-72000, enfuvirtide, erlotinib hydrochloride, escitalopram oxalate, etoricoxib; Fampridine, ferumoxytol, fondaparinux sodium; Gadofosveset sodium, gastrazole, gefitinib, gemtuzumab ozogamicin, gepirone hydrochloride glutamine; hLM609, HSPPC-96, human insulin; IDD-1, imatinib mesylate, indisulam, inhaled insulin, ixabepilone; Keratinocyte growth factor; Lapatinib, laquinimod, LDP-02, LE-SN38, levetiracetam, levosimendan, licofelone, liposomal doxorubicin, liposomal NDDP, lopinavir, lumiracoxib, LY-156735; Morphine hydrochloride, morphine-6-glucuronide, motexafin gadolinium, MS-27-275, MVA-5T4, MVA-Muc1-IL-2; Nemifitide ditriflutate, neridronic acid nitronaproxen, NSC-683864, NSC-703940, NVP-LAF-237; Oblimersen sodium, ocinaplon, oncomyc-NG, OPC-28326, ortataxel, ospemifene; Palonosetron hydrochloride, PEG-filgrastim peginterferon alfa-2(a), peginterferon alfa-2b, pegsunercept, pemetrexed disodium, pregabalin, prilocaine, pyridoxamine; RDP-58, recombinant glucagon-like peptide-1 (7-36) amide, recombinant human ApoA-I milano/phospholipid complex; SB-715992, soblidotin, sodium dichloroacetate, St. John's Wort extract; TAS-102, terfenadine, TG-1024, TG-5001, 4'-Thio-ara-C, tipranavir, topixantrone hydrochloride, trabectedin, transdermal selegiline, trimethoprim, troxacitabine, TT-232; Vatalanib succinate, vinflunine; Ximelagatran; Ziprasidone hydrochloride, Zoledronic acid monohydrate.
 ...
PMID:Gateways to clinical trials. 1498 42