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)

The effects of intravenous infusion of arginine (20 g/m2) after an overnight fast on plasma immunoreactive growth hormone (GH), insulin (IRI), and glucagon (IRG), and blood glucose were examined in five groups of children and adolescents: 10 normal individuals, 18 with idiopathic short stature, 6 with isolated growth hormone deficiency, 8 with panhypopituitarism, and 6 with anorexia nervosa. The mean fasting plasma GH concentration was significantly elevated in the group with anorexia nervosa (P less than 0.05), and similar to the value for the normal group in all other groups. After arginine infusion, four- to sixfold increases of plasma GH were observed in the normal children, and similar increases were seen in those with idiopathic short stature as well as in those with anorexia nervosa; whereas, in the children with isolated growth hormone deficiency or panhypopituitarism, there was no significant increase in plasma GH. Fasting blood glucose concentrations were significantly lower than normal in subjects with isolated growth hormone deficiency (P less than 0.05), panhypopituitarism (P less than 0.001), and anorexia nervosa (P less than 0.001), whereas fasting plasma IRI and IRG concentrations were similar to the values in the normal group. Plasma IRI increased eightfold at the end of the 30-min arginine infusion in the normal subjects; the increase was slightly but not significantly less in those with idiopathic short stature, and significantly less in those with isolated growth hormone deficiency (P less than 0.05), panhypopituitarism (P less than 0.001), and anorexia nervosa (P less than 0.05). Arginine infusion resulted in two- to threefold increases of plasma IRG in the normal group, and similar increases were observed in all of the other groups tested. These results suggest that whereas pancreatic beta cell responsiveness may be deficient in children and adolescents with isolated growth hormone deficiency, panhypopituitarism, or anorexia nervosa, pancreatic alpha cell responsiveness, to arginine at least, appears to be intact under these conditions.
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PMID:Plasma growth hormone, insulin, and glucagon responses to arginine infusion in children and adolescents with idiopathic short stature, isolated growth hormone deficiency, panhypopituitarism, and anorexia nervosa. 110 71

A boy with neonatal hypoglycemia, genital hypoplasia and frontal prominence ahd recurrence of hypoglycemic seizures at age 17 months. There was no plasma growth hormone (GH) response to sleep, arginine, hypoglycemia or glucagon. Mild secondary hypothroidism and primary hypogonadism were demonstrated. Small dose testosterone therapy for three months resulted in normal penile size; weekly injections of GH accelerated linear growth to a normal pace. Whether this complex represents a true syndrome or part of the spectrum of panhypopituitarism remains to be answered.
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PMID:Growth hormone deficiency with hypoglycemia, genital hypoplasia and frontal prominence. 447 Aug 95

We reported a boy with panhypopituitarism after removal of a suprasellar teratoma and pituitary stalk transection at the age of 3 months. His growth was accelerated after 5 years of age without growth hormone (GH) therapy, although he had poor height growth until age 4 under treatment with hydrocortisone, levothyroxine sodium, and desamino-D-arginine vasopressin (DDAVP). Hyperphagia and obesity developed after surgery. Endocrinological examination revealed no GH response to glucagon, low serum levels of insulin-like growth factor (IGF)-1 and IGF binding protein-3 (IGFBP-3). Serum prolactin was normal, but serum insulin was high. Some patients who received an operation for craniopharyngioma were reported to achieve normal growth without GH secretion, but the mechanism is still unknown. High serum levels of prolactin or insulin can be associated with normal IGF in GH deficient patients. This patient had obesity and high serum insulin, which may be related to growth without GH secretion.
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PMID:A boy with normal growth in spite of growth hormone deficiency after resection of a suprasellar teratoma. 1089 Jan 95

To establish the diagnosis of adult growth hormone deficiency (GHD), GH-deficient children transitioning to adulthood are evaluated by two separate stimuli 2 or more weeks after ceasing GH therapy. While 20-88% of children diagnosed with idiopathic GHD retest with normal values, those with proven genetic defects in GH production/secretion/bioactivity and patients with panhypopituitarism consistently test deficient. The US Food and Drug Administration (FDA) defines GHD in adults by stimulated peak serum GH concentrations <5 ng/ml if measured by polyclonal radioimmunoassays (RIA) or lower if measured by monoclonal assays. Some investigators define severe GHD by a peak GH concentration <3 ng/ml. Adult responses to arginine and glucagon testing are similar to the responses to insulin tolerance testing; clonidine, pyridostigmine, and galanin cause lesser peaks of GH. Growth hormone-releasing hormone (GHRH) combined with arginine, GH releasing peptide-6 (GHRP-6), or hexarelin leads to higher peak responses than GHRH alone. Thus the choice of testing methods impacts the diagnosis of GHD in transition patients.
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PMID:A practical approach to the diagnosis of growth hormone (GH) deficiency in patients transitioning to adulthood using GH stimulation testing. 1279 66

The insulin tolerance test (ITT) is considered the test of choice for the diagnosis of GH deficiency (GHD). However, in patients with contraindications to ITT, alternative provocative tests must be used with appropriate cut-offs. The glucagon stimulation test has proved to be a safe, low-cost and effective means of stimulating GH secretion, and therefore can be considered as a suitable alternative to the ITT. We have studied the GH response to the glucagon test in 33 patients with known pituitary disease, 12 males and 21 females, aged between 21 and 60 yr (41.18 +/- 9.47 yr); 5 had isolated GHD and 28 had panhypopituitarism. We also evaluated a control group of 25 individuals, matched for age and sex (8 males and 17 females), aged between 20 and 60 yr (39.28 +/- 12.10 yr). They were selected via the ITT if their peak GH response was > 5.0 ng/ml. GH peak after glucagon was significantly lower in the group of patients compared to the control group (0.49 +/- 0.85 vs 8.69 +/- 5.85 ng/ml, p = 0.0001). Receiver-operating characteristic (ROC) plot analyses of the control and GHD group showed an area under the curve of 0.982 for GH peak response to glucagon. The response value of 3.0 ng/ml showed the best pair of sensitivity (97%)/specificity (88%), and was chosen as the cut-off defining GHD. After evaluation of positive predictive values (PPV) and negative predictive values (NPV) through simulation of different prevalences of the disease, we concluded that the cut-off point of 3.00 ng/ml maximizes both PPV and NPV (100%). In conclusion, we have shown that the glucagon stimulation test has a good performance and great diagnostic accuracy for the diagnosis of GHD.
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PMID:Glucagon stimulation test for the diagnosis of GH deficiency in adults. 1500 42

GH deficiency (GHD) in adults has to be shown by a single provocative test, provided that it is validated. Insulin tolerance test (ITT) has been indicated as the test of choice; now also glucagon test is validated and represents an alternative. The GHRH plus arginine (ARG) test and testing with GHRH plus a GH secretagogue are equally reliable diagnostic tools, and are now considered as 'golden' standards as ITT. Childhood-onset (CO) GHD needs retesting in late adolescence or young adulthood; this is a major clinical challenge and raises questions about the most appropriate method and cut-off value. Appropriate re-evaluation of GH status is represented by simple measurement of IGF1 concentration off rhGH treatment. Clearly, low IGF1 levels are evidence of persistent severe GHD in subjects with genetic GHD or panhypopituitarism. However, normal IGF1 levels never rule out severe GHD and CO-GHD with normal IGF1 levels must undergo a provocative test. The appropriate GH cut-off limit is specific for each provocative test. As shown by the ROC curve analysis, in late adolescents and young adults, the lowest normal GH peak response to ITT is 6.1 microg/l while that to GHRH+ARG test is 19.0 microg/l. These cut-off limits, however, are just indicative as being variable as a function of the assay used. No other test is validated for retesting. As GHRH+ARG test mostly explores the GH-releasable pool, normal GH response would be verified by a second ITT in order to rule out subtle hypothalamic defect.
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PMID:Retesting the childhood-onset GH-deficient patient. 1880 14