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 specific binding of 125I-labeled insulin, human hormone ([125I]hGH), bovine growth hormone ([125I]bGH), and ovine prolactin ([125I]oPRL) was studied in mouse liver membranes. [125I]hGH and [125I]oPRL bound to adult liver membranes. Pregnancy increased the specific binding of [125I]hGH but not that of [125I]oPRL. [125I]hGH was displaced from membranes of pregnant mice by hGH, oPRL, and bGH, but only by hGH and oPRL from liver membranes of nonpregnant mice. Significant specific binding of [125I]bGH was seen only in pregnancy. The binding of [125I]bGH to pregnant mouse liver membranes increased with increasing concentration of either membrane protein or [125I]bGH. Both the specific binding and dissociation of [125I]bGH were greatly influenced by the time and temperature of incubation. Binding of [125I]bGH was inhibited by growth hormones, including hGH and rat GH, and not by lactogenic hormones (various prolactins and human placental lactogen), ACTH, glucagon, or insulin. The inhibition of [125I]hGH binding by hGH and bGH, in the presence of excess (2 mug/ml) of PRL, was very similar to that seen with [125I]bGH. Scatchard plots of displacement dose-response curves obtained under steady state conditions of 4C were nonlinear and very similar with either [125I]bGH or [125I]hGH. This contrasted with the linear Scatchard plots obtained from displacement dose-response curves of either [125I]oPRL or [125I]hGH in the presence of excess (2 mug/ml) bGH. Termination of pregnancy, either naturally or by hysterectomy, reduced [125I]bGH specific binding to nonpregnant levels by 24 to 36 h. Estrogen administration did not increase [125I]bGH binding in hepatic membranes. Nonpregnant mice possess hepatic lactogen binding sites which are uninfluenced by pregnancy. GH specific binding sites are markedly augmented during pregnancy. The close correlation between the level of these sites and pregnancy suggests that they are regulated by a product of the fetoplacental unit.
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PMID:Characterization and modulation of growth hormone and prolactin binding in mouse liver. 17 65

The amount of cAMP in the pubic symphyses of estrogen-primed mice increases after injection of the hormone relaxin. This relaxin-induced increase in symphyseal cAMP was observed in immature, mature, and ovariectomized mature mice and could be prevented by prior ip injection of rabbit antibodies to porcine relaxin or by treatment of relaxin with dithiothreitol. The highest level of cAMP was measured 30 min after relaxin injection; the level of measurable cMAP then diminished rapidly. Estrogen-priming of the mice was not a prerequisite for a relaxin-induced response to occur. Relaxin administration did not increase the level of cAMP in a non-target tissue such as liver, nor could an increase in cAMP in the pubic symphysis be elicited by injection of insulin, a protein of similar size and structure, or glucagon, a known stimulator of liver cAMP levels.
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PMID:Relaxin-dependent adenosine 6',5'-monophosphate concentration changes in the mouse pubic symphysis. 21 19

The effect of medroxyprogesterone acetate (MPA) on basal circulating lipids, arginine-stimulated glucagon and insulin secretion, and glucose tolerance was studied in normal women. After 5 days of oral MPA treatment (10 mg/day), there was a small but significant decline in basal circulating triglycerides. No changes were observed in fasting plasma concentrations of cholesterol, free fatty acids, glucagon, insulin, or glucose; in the plasma glucagon, insulin, or glucose responses during L-arginine infusion; or in the plasma insulin or glucose responses during oral glucose tolerance tests. There was no correlation of any of these parameters with the observed decline in fasting plasma triglyceride concentrations. These results confirm previous reports of no consistent changes in lipid or glucose homeostasis in women using derivatives of 17alpha-acetoxyprogesterone derivatives for contraceptive purposes, and suggest that MPA may be a suitable alternative for those women who develop hyperlipemia or glucose intolerance when they use contraceptive agents which contain derivatives of ethinyl estradiol and nortestosterone.
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PMID:Effect of contraceptive steroids on arginine-stimulated glucagon and insulin secretion in women. III. Medroxyprogesterone acetate. 90 95

To evaluate the effect of contraceptive steroids on endogenous glucagon and insulin secretion, theta-arginine was infused intravenously in normal young women before and during selective steroid treatment. The effect of the combination of an estrogen derivative (mestranol), plus norethindrone (Norinyl, Syntex) was compared to the effect of ethinyl estradiol alone and to norethindrone alone. All three steroid schedules resulted in suppression of aminogenic insulin secretion. However, glucagon secretion was reduced only with ethinyl estradiol alone or the combination of mestranol plus norethindrone. In accordance with previous reports, treatment with an ethinyl estradiol derivative alone or in combination with norethindrone resulted in a tendency for elevated serum lipid concentration, while norethindrone alone resulted in a significant reduction in serum lipid concentration. These observations suggest an inverse relationship between aminogenic glucagon secretion and serum lipid concentration as influenced by contraceptive steroids. It is suggested that the metabolic effects of these steroids may be mediated in part by the associated alterations in pancreatic hormone secretory capacity.
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PMID:Effect of contraceptive steroids on arginine-stimulated glucagon and insulin secretion in women: I-Lipid physiology. 115 75

Progesterone receptors (PgR) have been immunocytochemically localized in the nuclei of several (40% to 75%) endocrine cells of the human pancreas and in a more variable number of neoplastic cells of 7 of 18 endocrine pancreatic tumors. Conversely the exocrine epithelial cells of the pancreas did not exhibit any PgR immunoreactivity in normal as well as in different pathologic conditions, including pancreatic adenocarcinomas. Estrogen receptors were not detected in any of the pancreatic samples investigated. Double immunocytochemical experiments have documented that PgR immunoreactivity in normal Langerhans islets is a consistent feature of most (75%) glucagon-producing A cells, of approximately 5% to 20% of insulin-producing B cells, and of a variable percentage of pancreatic polypeptide (PP)-producing cells, ranging from 5% to 70%. These figures were not affected by the sex, age, or underlying disease of the patients. The reported findings corroborate previous clinical and experimental evidence indicating that sex steroid hormones may have some regulatory effects on the functional activity of the endocrine pancreas.
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PMID:Immunocytochemical localization of progesterone receptors in endocrine cells of the human pancreas. 224 Jan 68

The effect of a low-dose triphasic oral contraceptive (ethinyl estradiol and levonorgestrel) on glucose tolerance, plasma insulin and glucagon responses to glucose, fasting plasma cortisol, triglycerides, free fatty acids, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and very--low-density lipoprotein cholesterol was investigated in 16 women with previous gestational diabetes and in 19 normal women. Investigations were performed prior to the hormonal intake and after treatment for 2 and 6 months. Before treatment, the women with previous gestational diabetes had significantly elevated fasting glucose (p less than 0.05) and impaired glucose tolerance (p less than 0.05) when compared to those of the healthy control subjects. The glucose, insulin, and glucagon responses to oral glucose remained unchanged during the treatment period. Plasma cortisol increased in both groups (p less than 0.05) whereas plasma triglycerides increased in the control subjects only (p less than 0.05). Plasma free fatty acids, lipoproteins, and high-density lipoprotein cholesterol/total cholesterol ratio remained unchanged in both groups. The results suggest that a low-dose triphasic oral contraceptive (ethinyl estradiol and levonorgestrel) is suitable as contraception even in women with a previous deterioration of glucose tolerance during pregnancy.
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PMID:Triphasic oral contraception: metabolic effects in normal women and those with previous gestational diabetes. 393 51

The carbohydrate metabolic status in 10 women with previous non-insulin-dependent diabetes in pregnancy and in 8 control subjects was evaluated prospectively during a 6-month treatment period with an oral contraceptive containing 30 micrograms ethinyl estradiol and 150 micrograms levonorgestrel. An oral glucose tolerance test was performed before treatment and after tablet intake for 2 and 6 months. At each test, plasma values of glucose, insulin, and glucagon were measured. Before treatment the non-insulin-dependent diabetic patients demonstrated significantly increased glucose values and decreased insulin values as compared with the values of the control subjects. During treatment they displayed a small but significant rise in plasma insulin values. The glucose tolerance, however, remained unaffected in both groups during the study period. No change in body weight or blood pressure was observed. The results indicate that hormonal contraception of the low dosage type may be administered to women with previously impaired glucose tolerance in pregnancy without any deterioration of the glucose metabolism post partum.
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PMID:Low dosage oral contraception in women with previous gestational diabetes. 680 1

Synthesis of rat liver histidase is under multihormonal control; estrogen, glucocorticoid, and glucagon, via cAMP, induce this enzyme. By means of in vivo [3H]leucine incorporation into immunoprecipitated histidase, relative to that incorporated into total soluble protein, we have now demonstrated that de novo hepatic histidase synthesis, as well as catalytic activity, is selectively increased following hypophysectomy. Treatment of hypophysectomized rats with physiological levels of triiodothyronine (T3) diminished histidase synthetic rates and catalytic activities to normal levels, despite concomitant elevation in total soluble protein synthesis. Thyrotoxic doses of T3 further reduced histidase synthesis to barely measurable rates. Since thyroid hormone is under pituitary regulation, this hormone may be primary in the hypophyseal suppression of histidase. Estrogen does not induce hepatic histidase in the hypophysectomized rat. However, administration of the histidase suppressor, T3, or prolactin, which in itself has no effect on this enzyme, was ineffective in reinstating estrogen inducibility of histidase in the hypophysectomized animal. Thus, some as yet unknown hypophyseal agent is required for estrogenic inducibility of this liver enzyme.
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PMID:Effects of hypophysectomy and triiodothyronine on de novo biosynthesis, catalytic activity, and estrogen induction of rat liver histidase. 739 Oct 78

11 oophorectomized women (mean age 34.5 + or - 5.9) were given the 17-C-alkylate (EE) ethinyl estradiol 20 mcg/day and the nonalkylated estrogen, (E2V) estradiol valerianate 2 mg/day for 6 weeks in separate periods preceded by 6 weeks without hormonal replacement therapy. Blood samples were drawn before and after 6 weeks on each estrogen. Serum phospholipids, cholesterol, and triglycerides were assessed. Preparative ultracentrifugation with the isolation of the very low density (VLDL; d 1.006 g/ml); the low density (LDL; d-1.006, 1.063 g/ml), and the high density lipoprotein (HDL; d 1.063 g/ml) fraction was carried out. In the 3 lipoprotein fractions, phospholipid, total cholesterol, free cholesterol, and triglycerides were determined. An oral glucose tolerance test with concomitant plasma insulin determinations was performed. In the present study, EE caused an increase in serum total and LDL triglycerides while there was a reduction of triglycerides in serum as well as in VLDL and LDL when E2V was administered. This finding supports earlier studies indicating that insulin (or rather the insulin-glucagon relationship) influences the hepatic triglyceride productionr ate. Both EE and E2V increased HDL cholesterol but E2V did not induce a concomitant increase in serum triglycerides which would suggest a more physiological effect from the latter compound since fertile females have lower serum triglycerides and higher HDL cholesterol levels than males of the corresponding age. The same differences are true in a comparison between fertile and postmenopausal women.
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PMID:Lipid metabolic studies in oophorectomized women: effects induced by two different estrogens on serum lipids and lipoproteins. 743 9

We studied the influence of glucagon on hepatic LDL receptors and plasma lipoproteins in rats. A dose-dependent (maximum, threefold) increase in LDL-receptor binding was evident already at a dose of 2 x 4 micrograms, and detectable 3 h after injection; concomitantly, cholesterol and apolipoprotein (apo) B and apoE within LDL and large HDL decreased in plasma. LDL receptor mRNA levels were however unaltered or reduced. Hepatic microsomal cholesterol was increased and the enzymatic activities of 3-hydroxy-3-methylglutaryl coenzyme A reductase and cholesterol 7 alpha-hydroxylase in hepatic microsomes were reduced. Insulin alone increased receptor binding and receptor mRNA levels twofold, but plasma cholesterol was unchanged and plasma apoE and apoB increased. Administration of insulin to glucagon-treated animals reduced the LDL-receptor binding to control levels and apoB appeared in LDL particles. Estrogen treatment increased LDL-receptor binding and mRNA levels five- and eightfold, respectively. Combined treatment with glucagon and estrogen reduced the stimulation of LDL-receptor mRNA levels by 80% although LDL-receptor binding was unchanged. Immunoblot analysis showed that glucagon increased the number of hepatic LDL receptors. We conclude that glucagon induces the number of hepatic LDL receptors by a mechanism not related to increased mRNA levels, suggesting the presence of a posttranscriptional regulatory mechanism present in the liver in vivo.
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PMID:Stimulation of rat hepatic low density lipoprotein receptors by glucagon. Evidence of a novel regulatory mechanism in vivo. 851 87


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