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 aim of this study was to assess the acute effects of clonidine, an alpha 2-adrenergic agonist, on hormonal responses to graded exercise in 8 healthy young men. After fasting overnight, each subject was tested on 2 mornings, 1 week apart. On one occasion he was given 200 micrograms clonidine orally and on the other identical placebo tablets, the order being randomized in a double-blind fashion over the 2 days. Thereafter each subject performed 2 successive treadmill runs, equivalent to 60 and 100%, respectively, of maximal aerobic power. Clonidine pretreatment blunted the maximal increase in plasma catecholamines by more than 60% of the control response (p less than 0.01), without significantly altering the rise of plasma cortisol or ACTH. Furthermore, clonidine significantly reduced the exercise-induced maximal rise in plasma glucose, without modifying the slight decline in mean plasma insulin or increase in pancreatic glucagon levels. The drug did not affect the maximal increments in plasma growth hormone or prolactin occurring after exercise. It was concluded that a single dose of clonidine suppressed peripheral sympathetic responses, without altering central (pituitary) alpha-adrenergic-mediated hormonal responses, to short-term exercise in healthy men.
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PMID:Clonidine and the hormonal responses to graded exercise in healthy subjects. 300 52

A 54 year old woman suffered from acromegaly due to a pancreatic islet cell tumour producing GHRH. The tumour was demonstrated on CT scan. The diagnosis was established from elevated plasma levels of GHRH, GH and prolactin, and by the lack of signs of a pituitary adenoma in trans-sphenoidal surgery. Acromegaly was cured by tumour removal. Light microscopically, the tumour showed a medullary and microlobular pattern. The cells were large and often cuspidal. Small granules were found in semi-thin sections. Small aggregations of amyloid fibres were seen, mostly around capillaries. Immunocytochemistry revealed GHRH, NSE, neurotensin, serotonin, VIP and PP. S 100 was positive only in nerve fibres. Staining for GH, ACTH, calcitonin, alpha-HCG, beta-HCG, insulin, glucagon, gastrin, substance P, bombesin and somatostatin was negative. Ultrastructure showed oval partly lobulated nuclei with small nucleoli, moderate amounts of rough endoplasmic reticulum, many free ribosomes, some large Golgi fields and small numbers of secretory granules measuring 150 nm or, in a few cells, 650 nm. Only 4 other cases of pancreatic endocrine tumours causing acromegaly by ectopic GHRH secretion are described in the literature and these were similar to our case in many respects.
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PMID:Morphology of a GHRH producing pancreatic islet cell tumour causing acromegaly. 301 79

Growth hormone-releasing factor (GRF) stimulates the release of growth hormone from the anterior pituitary and is related to the peptides of the glucagon/secretin family. Although the mechanism of action of this hormone has been studied in considerable detail, little is known concerning the GRF receptor itself. We have attempted to label the GRF receptor by chemically coupling the 125I-GRF analog [His1, Nle27]-hGRF(1-32)-NH2 (GRFa) (where Nle is norleucine) to plated rat anterior pituitary cells with the protein cross-linker disuccinimidyl suberate (DSS) (0.1 mM). Verification of biological activity of the 125I-GRFa was confirmed prior to the cross-linking experiments using the reverse hemolytic plaque assay. Whole cell extracts prepared from the cross-linked cells were subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by autoradiography of the dried gels. Four bands of 72, 50, 30, and 26 kDa were detected in autoradiograms from cells exposed to the labeled analog for 20 min (22 degrees C) followed by exposure to DSS for 2 min. The 72-kDa band was interpreted to be bovine serum albumin, which was used as a carrier in initial studies. The 50- and 30-kDa bands were very faint and probably represent nonspecific binding sites since they were unchanged in the presence of excess unlabeled GRFa. The 26-kDa band was diminished in a concentration-dependent manner by unlabeled rat GRF, GRFa, and to a lesser extent by vasoactive intestinal peptide (VIP). It is unlikely, however, that GRFa was acting at a VIP receptor since the labeled analog did not induce prolactin secretion (VIP is a prolactin secretagogue). GRFa also increased cellular cAMP to levels similar to GRF and greater than VIP. Autoradiographs from gels run under nonreducing conditions revealed the 26-kDa band as the major species, indicating that, if a polymeric form of this binding protein exists, it does not involve disulfide linkages. Thus, the best candidate for the putative GRF receptor is the 26-kDa band. We have further demonstrated that the higher concentrations of DSS used previously (5 mM) result in diffuse autoradiograms with multiple bands, suggesting that caution should be exercised when interpreting cross-linking data under these conditions.
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PMID:Cross-linking of a growth hormone releasing factor-binding protein in anterior pituitary cells. 302 63

Effect of insulin on glucagon binding to rat epididymal adipocytes was studied in vitro. [125I]iodoglucagon binding to isolated adipocytes was increased by preincubation of the cells with insulin. Maximal increase was observed with 7 X 10(-10) M insulin. In Scatchard analysis, [125I]iodoglucagon competition data generated one binding site with a single affinity for glucagon binding in the cells pretreated with buffer alone. Pretreatment of the cells with insulin increased the affinity without changes in the number of binding sites. [125I]iodoglucagon binding to isolated adipocytes was not affected by pretreatment of the cells with luteinizing hormone, follicle-stimulating hormone, growth hormone, or with prolactin. These results suggest that insulin stimulates glucagon binding to adipocytes.
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PMID:Effect of insulin on glucagon binding to isolated rat epididymal adipocytes. 302 93

Opiates stimulate the growth hormone and prolactin responses to stimuli in non-obese humans. Obese patients, however, show lowered growth hormone and prolactin responses and raised beta-endorphin levels. We therefore investigated the effect of the opiate antagonist naloxone on the stimulated growth hormone and prolactin secretions in a controlled double-blind study in obese patients. All patients received 200 micrograms TRH and 0.5 g/kg b.w. arginine together with 2 mg of naloxone or placebo i.v. in a randomized sequence. The TRH- and arginine-induced increases in prolactin and growth hormone were significantly greater after administration of naloxone (p less than 0.05). Naloxone also produced a significant increase in ACTH, cortisol and beta-endorphin when compared with placebo. TSH, triiodothyronine, thyroxine, insulin, glucagon and blood glucose showed no significant differences between both days of the trial. The effect of naloxone on growth hormone and prolactin secretions in obese humans can thus be regarded as a partial normalization. We therefore conclude that the hypothalamic regulatory disturbance of growth hormone and prolactin secretions in the obese could be caused by raised opiate levels.
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PMID:Naloxone increases the response of growth hormone and prolactin to stimuli in obese humans. 303 2

In 72 patients with end-stage renal failure and 70 healthy subjects, the influence of blockade of opioid receptors by naloxone on secretion of prolactin, lutropin (LH), follitropin (FSH), adrenocorticotropin (ACTH), somatotropin (HGH), insulin (IRI), glucagon (IR-G), parathyroid hormone (PTH) and calcitonin (CT) was studied. Administration of naloxone stimulated luliberin-induced LH and FSH secretion quantitatively equally in patients and controls. Blockade of opioid receptors was followed by a less marked suppression of chlorpromazine-induced prolactin secretion but by a higher response of hypoglycemia-induced ACTH secretion in uremic patients than in controls. In addition, a less marked suppressive effect of naloxone was noted on hypoglycemia-induced HGH secretion in chronic renal failure as compared with controls. Blockade of opioid receptors improved significantly glucose tolerance and glucose-induced insulin secretion in uremic patients and suppressed nearly completely glucagon secretion response during the second phase of a glucose tolerance test. Finally, administration of naloxone was followed by a blunted response of Ca-induced CT secretion and suppression of PTH. Data presented in this paper suggest the existence of hyperendorphinism in end-stage renal failure.
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PMID:Effects of naloxone administration on endocrine abnormalities in chronic renal failure. 303 7

The existence of insulin receptors and biological responses to insulin on macromolecular synthesis have been studied in C6 glioma cells. Binding of 125I-insulin to C6 glioma cells was specific, time- and PH-dependent. Porcine insulin competed for 125I-insulin binding in a dose-dependent manner. Unlabeled polypeptides, including glucagon, bovine growth hormone, bovine prolactin did not compete for 125I-insulin binding. Scatchard analysis of the binding data gave a curvilinear plot which may indicate negative co-operativity or the existence of both high and low affinity (Ka = 7.55 x 10(10) - 4.25 x 10(9] sites. Incubation of cultures with insulin caused a time and dose-dependent stimulation of DNA, RNA and protein synthesis in C6 glioma cells (measured by 3H-thymidine, 3H-uridine or 3H-leucine incorporation into DNA, RNA, or protein respectively). The increase of macromolecular synthesis was admitted at more than 2 nM concentration of insulin. Maximal stimulation of DNA synthesis (142% of control) occurred 6 hours after incubation with 167 nM insulin. The same concentration of insulin caused a 45% increase in 1 hour on RNA synthesis, a 37% increase in 2 hour on protein synthesis. These results indicate that C6 glioma cells have specific insulin receptors capable of mediating effects of insulin on macromolecular synthesis. Insulin in the brain and even blood may be an important growth factor in the glioma cells of the patients with disrupted blood-brain-barrier.
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PMID:Insulin binds to specific receptors and stimulates macromolecular synthesis in C6 glioma cells. 304 34

1. The present paper reports the effects of dietary modifications on the diurnal pattern of concentrations of certain metabolites and hormones in the peripheral blood of lactating dairy cows. The cows were given fixed rations of hay and high-cereal concentrates in the proportions of 30:70 or 10:90 (w/w). The concentrates were given in either two or six equal meals daily; the hay was given twice daily. 2. Previous reports of the same experiment had shown that milk-fat yield and concentration were reduced by increasing the proportion of concentrates in the diet and increased by more frequent feeding of the concentrates. These changes could be explained in part by changes in rumen volatile fatty acid (VFA) proportions and mean daily concentrations of VFA, particularly propionic acid, and insulin in the peripheral blood, but these factors failed to explain all the increase in milk-fat concentration caused by more frequent feeding. 3. Analysis of blood samples taken at hourly intervals for 24 h at two stages of lactation showed that, in the cows fed six times daily, the concentrations of metabolites and hormones remained relatively constant over the day. In the cows fed twice daily, the concentrations of VFA, 3-hydroxybutyric acid and insulin all increased after both meals whereas the concentrations of glucose and growth hormone tended to fall. The concentration of non-esterified fatty acids tended to increase overnight and fall rapidly after the morning feed. The concentrations of glucagon, thyroxine and prolactin showed no clear pattern in relation to meals. The postprandial responses of propionate, insulin and growth hormone were greater with the higher concentrate diet. 4. The maximum concentration and the diurnal range of concentrations were reduced by more frequent feeding of both diets in the case of propionic acid and of the higher concentrate diet in the case of insulin, but the effects on insulin concentrations of more frequent feeding of the lower concentrate diet were smaller and not significant. The maximum concentration and the diurnal range of concentrations of growth hormone were unaffected by meal frequency. 5. It is concluded that the severity of milk-fat depression in cows fed twice daily is increased by the rapid rise in propionic acid concentration in the peripheral blood after a meal, which in turn increases insulin secretion and may be accompanied by a suppression of growth hormone release. This causes lipogenesis to be diverted towards adipose tissue at the expense of the mammary gland.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Feeding frequency for lactating cows: diurnal patterns of hormones and metabolites in peripheral blood in relation to milk-fat concentration. 305 1

Controversy exists over differences in hormonal counterregulatory (CR) responses to human and porcine insulins with conflicting reports regarding the adrenaline, glucagon, growth hormone, cortisol and prolactin responses to the two species of insulin. It has been suggested that these differences may represent different central nervous system sensitivities to the two types of insulin. The CR responses to an intravenous bolus of 0.1 U/kg of neutral soluble semi-synthetic (SSHI) and biosynthetic (BHI) human insulins, porcine insulin and diluting medium as control were compared in six fasted normal male subjects. The plasma glucose fell similarly with all three insulins reaching a mean nadir of 1.5 +/- 0.2 mmol/l at 25 min. Peak responses to porcine, SSHI and BHI, respectively were: adrenaline--523 +/- 101, 424 +/- 62, 379 +/- 76 pg/ml; glucagon--0.064 +/- 0.01, 0.063 +/- 0.01, 0.078 +/- 0.01 nmol/l; cortisol--507 +/- 42, 539 +/- 65, 507 +/- 42 nmol; growth hormone--76 +/- 10, 76 +/- 5, 64 +/- 15 mU/l; prolactin--507 +/- 72, 608 +/- 103, 523 +/- 118 mU/l. These differences in CR response were not statistically significant. The results do not support the suggestion of a different hormonal counterregulatory response or central nervous system sensitivity to human and porcine insulins when administered by intravenous bolus injections to normal subjects.
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PMID:Hormonal counterregulatory responses to human (semi-synthetic and recombinant DNA) and porcine insulin induced hypoglycaemia. 306 61

In order to evaluate the effects of oral contraceptives on metabolic and endocrine function in teenagers, Norinyl 1/50 was begun in 46 12-17-year-old girls after a 16-hour-fasting flood sample was obtained for glucose, insulin, glucagon, growth hormone, lutenizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone, prolactin, gluconeogenic substrates, total lipids, and cholesterol. Sampling was repeated at 6 and 12 months of therapy. Of the 46 patients enrolled in the study, 23 returned for follow-up after 6 months, and 13 completed the study. Blood sampling after 6 and 12 months of therapy demonstrated no significant changes (p 0.05). Our results suggest that there were no changes in the metabolic or endocrine functions studied at 6 and 12 months on a medium-dose contraceptive agent. Study participants had requested an oral contraceptive and informed consent was obtained from all participants and their parents or guardians. The 36 black and 10 white patients ranged in age from 12.17 to 17.08 years with a mean of 15.0 years. Sexual development was Tanner stage 4 or 5. Mean gynecologic age was 2.83 years.
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PMID:The influence of oral contraceptives on hormonal and metabolic homeostasis in young adolescents. 318 64


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