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)

In 7 acromegalic patients growth hormone responses were studied following administration of synthetic TRF, propranolol-glucagon, insulin, and glucose p.o. Except for the glucose tolerance test, a good reproducibility of the STH response was observed. In 5 out of the 7 patients, there was a distinct rise in the plasma STH level after TRF. All patients with a positive insulin tolerance test responded to TRF, as did the two late responders to glucagon; the early responder to the latter test did not respond to TRF. It has been suggested (Liuzzi et al. 1974a) that TRF might be used as a screening test for detecting hypothalamic dependency of the acromegaly. This study suggests that further study is required before accepting this hypothesis and that a response to a combination of tests (TRF, glucagon, insulin) might be a better screening method.
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PMID:Comparison of TRF, propranolol-glucagon, insulin and glucose stimulation tests in acromegaly. 40 15

The association of hypoglycemia and microphallus in the male neonate is presumptive evidence of congenital hypopituitarism. This was observed in four male infants with normal birth weight and length, optic discs, and intelligence, and without gross central nervous system malformations. Plasma and urinary cortisol values were low. Stimulation with metyrapone and insulin hypoglycemia failed to elicit a rise in plasma corticoids, but multiple doses of ACTH evoked a response. Growth hormone responses to arginine, insulin, sleep, L-dopa, and glucagon were uniformly less than 2.5 ng/ml. In three patients, however, length remained within 2 SD of the mean until two years of age; in one, there was a sharp decrease in growth by three months. Two patients had low plasma TSH and thyroxine concentrations within the first month of life. In the other two patients, whose thyroxine levels were measurable, intravenous administration of thyrotropin-releasing factor evoked a normal rise in plasma TSH; serum thyroxine decreased into the hypothyroid range in one after GH therapy was initiated. Plasma prolactin was normal in the first two patients receiving thyroxine replacement therapy. The other two patients had elevated baseline prolactin levels and had an augmented rise in plasma prolactin after administration of TRF. Human chorionic gonadotropin induced a 10- to 15-fold rise in plasma testosterone in the two patients tested. The changes in plasma FSH and LH after luteinizing hormone-releasing factor were either low or in the prepubertal range. In three patients, treated with testosterone enanthate intramuscularly, phallic growth occurred. In addition, all three had a transient increase in height but no acceleration of skeletal maturation. The data suggest a deficiency of hypothalamic hypophysiotropic hormones rather than a primary pituitary defect. Early recognition of this syndrome complex is critical for prompt treatment of the life-threatening cortisol deficiency. The diagnosis is more difficult in affected females because their external genitals are normal. The microphallus is a remediable manifestation of hypopituitarism.
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PMID:Congenital hypopituitarism associated with neonatal hypoglycemia and microphallus: four cases secondary to hypothalamic hormone deficiencies. 118 16

The intracellular concentrations of cyclic AMP, polyphosphoinosides and free Ca2+ were unaffected during receptor-mediated endocytosis of the neoglycoprotein beta-D-galactosyl-bovine serum albumin (D-Gal-BSA) by isolated hepatocytes. Elevation of either intracellular cyclic AMP by glucagon or inositol phosphates and Ca2+ by vasopressin were without effect on the binding and internalization of D-Gal-BSA. The normal response of this cell to glucagon- and vasopressin-mediated mobilization of these second messengers was not modified in the presence of saturating concentrations of D-Gal-BSA. Receptor-mediated endocytosis of diferric transferrin (Fe3+-TRF) by both hepatocytes and HL60 cells was also shown to be independent of second messengers, although the unequivocal expression of the transferrin receptor by hepatocytes could not be satisfactorily demonstrated. The results of the present study are at variance with a suggested regulatory role for second messengers in receptor-mediated endocytosis of serum-derived ligands such as asialoglycoproteins and Fe3+-TRF. Receptor phosphorylation by protein kinase C in particular has been proposed to regulate the distribution and recycling of these receptors in actively endocytosing cells. We would suggest that if receptor phosphorylation has a regulatory role during endocytosis, it is likely to be mediated by a second-messenger-independent protein kinase analogous to casein kinase II. An alternative interpretation is that phosphorylation has no physiological significance and receptor-mediated endocytosis is a constitutive event coupled to membrane turnover.
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PMID:Receptor-mediated endocytosis of asialoglycoproteins and diferric transferrin is independent of second messengers. 254 88

Several neural peptides have been demonstrated to influence central nervous system control of nutrient metabolism. The principal mechanism by which these peptides influence peripheral nutrient metabolism is by altering the secretion of adrenal epinephrine. Bombesin or its mammalian counterpart, gastrin releasing peptide, and TRF act within the brain to stimulate the secretion of epinephrine from the adrenal gland. Associated with these changes in epinephrine secretion is a reduction of plasma insulin and elevation of plasma glucagon and glucose. Somatostatin and various somatostatin analogs act in the brain to inhibit adrenal epinephrine secretion stimulation by a variety of stimuli.
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PMID:Neuropeptides: central nervous system effects on nutrient metabolism. 611 88

Corticotropin-releasing factor (CRF) injected into the brains of rats produces hyperglycemia and an increase in plasma concentrations of glucagon, epinephrine, and norepinephrine. Neither hypophysectomy nor adrenalectomy prevents CRF-induced hyperglycemia. However, a role of adrenal epinephrine release in mediating CRF-induced hyperglycemia is supported by the finding that the central nervous system-selective somatostatin analog, desAA1,2,4,5,12,13-[D-Trp8]somatostatin, totally prevents the elevation of plasma epinephrine and suppresses the rise of plasma glucose but does not alter the increase in plasma norepinephrine induced by CRF. Pretreatment with the ganglionic blocker chlorisondamine completely prevents the CRF-induced rises in plasma glucose, epinephrine, and norepinephrine. These results demonstrate that CRF acts within the brain to stimulate sympathetic outflow, which results in the development of hyperglycemia. In contrast to other peptides that act within the central nervous system, e.g. bombesin, TRF, and beta-endorphin, whose hyperglycemic actions depend exclusively on adrenal epinephrine secretion, CRF-induced hyperglycemia is secondary to the enhanced secretion of both epinephrine and norepinephrine.
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PMID:Corticotropin-releasing factor: actions on the sympathetic nervous system and metabolism. 704 76

A tocotrienol-rich fraction (TRF(25)) and novel tocotrienols (d-P(21)-T3 and d-P(25)-T3) of rice bran significantly lowered serum and low density lipoprotein cholesterol levels in chickens. The present study evaluated the effects of novel tocotrienols on lipid metabolism in swine expressing hereditary hypercholesterolemia. Fifteen 4-mo-old genetically hypercholesterolemic swine were divided into five groups (n = 3). Four groups were fed a corn-soybean control diet, supplemented with 50 microg of either TRF(25), gamma-tocotrienol, d-P(21)-T3 or d-P(25)-T3 per g for 6 wk. Group 5 was fed the control diet for 6 wk and served as a control. After 6 wk, serum total cholesterol was reduced 32-38%, low density lipoprotein cholesterol was reduced 35-43%, apolipoprotein B was reduced 20-28%, platelet factor 4 was reduced 12-24%, thromboxane B(2) was reduced 11-18%, glucose was reduced 22-25% (P<0.01), triglycerides were reduced 15-19% and glucagon was reduced 11-17% (P<0.05) in the treatment groups relative to the control. Insulin was 100% greater (P<0.01) in the treatment groups than in the control group. Preliminary data (n = 1) indicated that hepatic activity of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase was lower in the treatment groups, and cholesterol 7alpha-hydroxylase activity was unaffected. Cholesterol and fatty acid levels in various tissues were lower in the treatment groups than in control. After being fed the tocotrienol-supplemented diets, two swine in each group were transferred to the control diet for 10 wk. The lower concentrations of serum lipids in these four treatment groups persisted for 10 wk. This persistent effect may have resulted from the high tocotrienol levels in blood of the treatment groups, suggesting that the conversion of tocotrienols to tocopherols may not be as rapid as was reported in chickens and humans.
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PMID:Novel tocotrienols of rice bran suppress cholesterogenesis in hereditary hypercholesterolemic swine. 1116 May 37

Several neural peptides have been demonstrated to influence central nervous system control of nutrient metabolism. The principal mechanism by which these peptides influence peripheral nutrient metabolism is by altering the secretion of adrenal epinephrine. Bombesin or its mammalian counterpart, gastrin releasing peptide, and TRF act within the brain to stimulate the secretion of epinephrine from the adrenal gland. Associated with these changes in epinephrine secretion is a reduction of plasma insulin and elevation of plasma glucagon and glucose. Somatostatin and various somatostatin analogs act in the brain to inhibit adrenal epinephrine secretion stimulation by a variety of stimuli.
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PMID:Neuropeptides: Central nervous system effects on nutrient metabolism. 2794 15