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)

An acquired partial pituitary insufficiency with selective ACTH and GH deficiency was demonstrated in two men aged 47 and 54, for which the clinical course over many years corresponds to Addison's disease. In one of the 2 cases, antibodies to anterior pituitary cell membrane, assayed by an immunofluorescence method with GH3 cells (rat GH and prolactin secreting cell) and AtT-20 cells (mouse ACTH secreting cell) as antigens, were positive. We also present a 55-year-old man with isolated ACTH deficiency associated with transient GH deficiency. In this case, hydrocortisone replacement corrected his subnormal, pre-therapy GH response to insulin tolerance and glucagon propranolol tests, although there was no response of serum GH to L-dops and arginine stimulation test before therapy. Selective ACTH and GH deficiency are very rare and the finding of transient GH insufficiency in a patient with isolated ACTH deficiency suggests that repeated testing while on hydrocortisone replacement therapy is of great diagnostic importance in order to distinguish between selective ACTH and GH deficiency and isolated ACTH deficiency accompanied by transient GH insufficiency.
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PMID:Reports of two cases of selective adrenocorticotropin (ACTH) and growth hormone (GH) deficiency: differential diagnosis from cases with isolated ACTH deficiency associated with transient GH insufficiency. 255 42

Data presented in this study suggest existence of hyperendorphinism in uraemic patients. This hyperendorphinism may be regarded both as a primary beneficial compensatory mechanism counteracting disturbances of the internal environment, while causing secondary harmful side effects, which contribute to the uraemic state. Erythropoietin treatment of uraemic, haemodialyzed patients is followed by marked endocrine alterations (suppression of plasma levels of STH, ACTH, prolactin, glucagon, aldosterone, cortisol and plasma renin activity, elevation of plasma insulin and atrial natriuretic levels, lack of influence on plasma PTH, CT and AVP). It remains to be clarified whether the erythropoietin induced endocrine alterations are due to correction of the existing anaemia or reflect a specific effect of this hormone.
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PMID:Endocrine abnormalities in patients with endstage renal failure. 256 Mar 46

The glucagon stimulation test (GST) is often used to assess pituitary ACTH reserve, particularly when other tests are contra-indicated. In a preliminary investigation, in patients with pituitary disease, we failed to demonstrate the ACTH dependence of the cortisol response. We have therefore compared the ACTH, cortisol and glucose responses to glucagon (1 mg s.c.), insulin (0.2 U/kg i.v., ITT) and placebo in six healthy male volunteers, sampling every 10 min for 6 h. During the GST, mean +/- SD serum cortisol rose from 256 +/- 80 nmol/l to a peak of 481 +/- 164 nmol/l (range 289-717 nmol/l, P less than 0.01) in comparison with 280 +/- 81 nmol/l to 602 +/- 110 nmol/l (range 493-742 nmol/l) during the ITT (P less than 0.002). The mean peak cortisol levels achieved in the two tests did not differ significantly. In the GST, plasma ACTH rose from a mean basal value of 10.9 +/- 16.6 ng/l to a mean peak level of 123 +/- 76 ng/l (P less than 0.02) (ACTH ng/l x 0.225 = pmol/l). The corresponding values in the ITT were 7.1 +/- 16.2 ng/l and 263 +/- 91 ng/l (P less than 0.001). The mean peak ACTH level was significantly greater during the ITT (P less than 0.05). Thus the cortisol response was ACTH dependent in both the GST and the ITT in normal subjects. Furthermore, the ACTH response was of sufficient duration to be detected by the usual procedure of sampling every 30 min.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of the ACTH and cortisol responses to provocative testing with glucagon and insulin hypoglycaemia in normal subjects. 256 Jun 84

Measurements of blood plasma ACTH, hydrocortisone, STH, somatostatin, insulin, glucagon levels and plasma renin activity in 70 patients with borderline hypertension (BAH) and in 20 normal male subjects have revealed increased ACTH, hydrocortisone, and somatostatin levels, elevated plasma renin activity, and reduced STH and insulin levels in the patients. A possible role of the pressor hormone system activation in the pathogenesis of borderline arterial hypertension and in BAH transformation into essential hypertension is discussed.
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PMID:[Hormonal disorders in borderline arterial hypertension]. 257 58

The microsomal brush-border fraction of rat renal tissue contains enzymatic activity, optimally active at pH 9, that is capable of degrading human myelin basic protein (BP) peptide 43-88. In the present study, this degradation and the effect on it of selected drugs and hormones were examined further. Of the substances tested, 10(-2) M chloroquine and 10(-5) M ACTH 1-24 were found to be the most effective inhibitors followed by 10(-5) M ACTH 1-39; parathormone, glucagon and insulin were found to be inhibitors an order of magnitude weaker than ACTH 1-24. Hydrocortisone, dexamethasone, maleic acid and ACTH 4-10 were found to have minimal or no inhibitory effect on the peptide degrading activity. Gel filtration of the degradation products indicated that the rate of degradation of BP peptide 43-88 at pH 9 had been retarded by ACTH 1-24. These studies indicate that the clearance and catabolism of this peptide may be altered by available therapeutic agents.
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PMID:Hormonal and drug effects on the degradation of human myelin basic protein peptide 43-88 by alkaline proteolytic activity in the rat kidney. 258 80

We investigated the effects of sevoflurane anesthesia and of surgery, on the endocrine functions as reflected by plasma levels of cortisol, aldosterone, ACTH, beta-endorphin-like immunoreactivity, prolactin, insulin, growth hormone, glucagon and glucose in surgical patients.
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PMID:Endocrine evaluation of sevoflurane, a new inhalation anesthetic agent. 262 72

A new syndrome in two siblings with primordial birdheaded nanism, progressive ataxia, goiter, primary gonadal insufficiency and insulin resistant diabetes mellitus is presented. Plasma concentrations of TSH, PTH, LH, FSH, ACTH, glucagon and insulin all working through cell membrane receptors were elevated. A generalized cell membrane defect was suggested to be the pathophysiological abnormality in these patients.
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PMID:Primordial birdheaded nanism associated with progressive ataxia, early onset insulin resistant diabetes, goiter and primary gonadal insufficiency. A new syndrome. 266 2

Radioimmunoassays of some hypophyseal, adrenal, thyroid, pancreatic, and sexual gland hormones, carried out in patients with pemphigus and bullous pemphigoid, have revealed increased levels of ACTH and hydrocortisone in their blood sera, vs. the reference values. Glucocorticoid therapy has normalized the ACTH level, and hydrocortisone content has proved to be below the norm. The blood plasma triiodothyronine level has been elevated, whereas insulin and glucagon lowered in the patients with pemphigus vs. those with bullous pemphigoid. In females of a menopausal age, suffering from pemphigus, increased levels of estradiol and reduced ones of testosterone have been detected, as compared to those suffering from bullous pemphigoid. These data evidence a varying functional activity of the endocrine glands in these dermatitides.
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PMID:[The hormonal profile of patients with pemphigus and bullous pemphigoid]. 268 71

The case history of a patient with serious hypoglycemia (with 0.6-3 mmol/l blood glucose) persisting for eight years and treated as epilepsy during the time of observation is reported. As the cause of hypoglycemia hyperinsulinemia, hypoglucagonemia, and moderate adrenal insufficiency was suggested. The pattern of secretion of insulin as well as of C-peptide indicated, that hyperinsulinemia was induced by hypersecretion of immunoreactive insulin. As the cause of hypersecretion of insulin insulinoma might have been ruled out. Hypoglucagonemia was shown by the low concentration of plasma glucagon. Adrenal insufficiency seemed to be due to ACTH deficiency. Replacement therapy with dexamethasone or administration of ACTH led to elevation of the blood glucose to normal, and the plasma cortisol also reached normal levels. On the basis of other data as well as of our own investigations we suggest a central origin of the illness. The patient has been free from his complaints with normal blood glucose and plasma cortisol concentrations for two years.
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PMID:Persistent hypoglycemia due to hyperinsulinemia, hypoglucagonemia and mild adrenal insufficiency. 282 82

We investigated the production, binding to cell membranes, and influence on cell proliferation of peptides and growth factors in 4 classic, 5 transitional, and 5 variant SCLC cell lines. Glucagon, neurotensin, and TGF-alpha were present in all cell lines. Bombesin was predominantly found in classic cell lines and insulin in variant cell lines. Neurokinin A, calcitonin, CGRP, GHRF, somatostatin, and CNTF were detectable in some cell lines without prevalence for a particular cell type. We could not detect AVP, growth hormone, neuropeptide Y, substance P, VIP, and NGF. Insulin binding sites were present on 11/14 cell lines, and some cell lines specifically bound bombesin, calcitonin, and EGF. Growth effects were detectable for insulin, GRP-related peptides, tachykinins, and VIP. Using serum-free conditions, insulin and VIP had a growth stimulating effect in liquid culture at nanomolar concentrations. Bombesin and neuromedin B stimulated the clonal growth at a concentration of 3-30 nM. The tachykinins neurokinin A, neurokinin B, physalaemin, and eledoisin inhibited the clonal and mass culture growth with a peak effect in the range of 0.1 to 10 pM. Peptide-induced stimulating and inhibiting effects were within a magnitude of 2-fold. All other peptides and growth factors tested, including ACTH, AVP, calcitonin, glucagon, neurotensin, somatostatin, EGF, CNTF, and NGF did not affect the growth of SCLC. We conclude that the growth of SCLC is partly controlled by such peptides in an autocrine/paracrine fashion.
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PMID:Peptides and growth factors in small cell lung cancer: production, binding sites, and growth effects. 283 87


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