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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Short term (30 min) infusion of cyclic somatostatin (50 microgram/rat), insulin (1 U/rat) or the two together significantly suppressed urinary cyclic AMP excretion in streptozotocin-diabetic rats. While somatostatin tended to increase cyclic GMP excretion, insulin had an opposite effect in diabetic but not in normal rats. It is suggested that somatostatin suppresses cyclic AMP excretion by inhibiting directly adenylate cyclase in liver and perhaps in other organs. The possibility that suppression of urinary cyclic AMP is due to inhibition of glucagon secretion is also considered.
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PMID:Somatostatin inhibits urinary cyclic AMP excretion in diabetic rats. 19 95

Glucagon administration to the intact rat has been shown to stimulate pyruvate metabolism in liver mitochondria, presumably by increasing pyruvate transport into the organelle. In this report, we used alanine in place of pyruvate to examine the possibility that glucagon might stimulate pyruvate carboxylation per se independent of its postulated action on pyruvate transport. In agreement with previous reports, injection of a low dose of glucagon (50 micrograms/kg of rat) increased respiration, ATP synthesis, pyruvate decarboxylation, and CO2 fixation in liver mitochondria subsequently isolated. When alanine was used as a substrate, CO2 fixation, but not decarboxylation, was increased in liver mitochondria isolated from glucagon-treated rats. Pyruvate accumulation under these conditions was significantly lower in the glucagon-treated rat preparation. When mitochondria were incubated in a HCO3- -deficient buffer, pyruvate accumulation was identical in both preparations. The addition of a pyruvate transport inhibitor, alpha-cyanohydroxycinnamate (0.5 mM), inhibited CO2 fixation with pyruvate by 70%, but had no effect when alanine was used. Our data therefore suggest that glucagon stimluates mitochondrial pyruvate carboxylation independent of its possible action on pyruvate transport.
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PMID:Glucagon stimulation of liver mitochondrial CO2 fixation utilizing pyruvate generated inside the mitochondria. 47 52

Hyperglycemia, hyperglucagonemia and hyperinsulinemia were observed in fasting rats at 0.5 hr after ip injection of NiCl2 (68 mumole per kg). Infusion of somatostatin iv (0.5 mg per rat) did not prevent Ni(II)-mediated hyperglycemia, hyperglucagonemia or hyperinsulinemia. Exposure of rats to inhalation of Ni(CO)4 (1.2 to 6.4 mumole per liter of air per 15 min) caused acute hyperglycemia, similar to that observed after ip injection of NiCl2. Hyperglycemia induced by NiCl2 and Ni(CO)4 was not associated with inhibition of erythrocyte glycolysis measured in vitro by erythrocyte uptake of 1-14C-glucose and release of 14CO2. These findings indicate that Ni-induced hyperglycemia may be mediated by increased pancreatic release of glucagon, but that Ni stimulation of glucagon release differs from stimulation of glucagon release by arginine or epinephrine, since the Ni effect is not antagonized by somatostatin.
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PMID:Effects of nickel chloride and nickel carbonyl upon glucose metabolism in rats. 73 12

During the first two thirds of gestation, the concentrations of UDPG, ATP, ADP, and Mg++ in human fetal liver remain constant, whereas the concentration of Pi decreases twofold and the G-6-P and AMP concentrations increase. Incubation of human fetal liver explants with glucagon or insulin did not alter the concentrations of any of these intermediates. ATP, ADP, and Pi are inhibitors of human fetal liver glycogen synthase D-form activity, while G-6-P and AMP and Mg++ are stimulators. Ca++ at concentrations of less than 0.1 mM was found to stimulate glycogen synthase D activity. This effect of Ca++ was also observed in "physiologic" mixtures containing UDPG, G-6-P, ATP, ADP, AMP, Pi, and Mg++ at concentrations found either in liver in utero or in explants. 45Ca++ efflux from perifused (rat) fetal liver explants was stimulated by glucagon. These data provide a picture of the metabolite regulation of human fetal liver glycogen synthase activity in which the D-form may largely control glycogen synthesis in utero and hormonal effects on glycogen synthase may be induced by effects of Ca++ on the D-form.
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PMID:Hormonal regulation of glycogen metabolism in human fetal liver. II. Regulation of glycogen synthase activity. 81 98

Coordinated studies have been carried out on the glucagon immunoreactive cells of the mammalian gastrointestinal tract (man, dog, rat), using electron microscopy, silver staining and immunocytochemistry. Parallel ultrastructural and immunocytochemical studies have been made with the semithin-thin serial section technique. The results indicate that while the glucagon cells of the oxyntic portion of the stomach are virtually indistinguishable from those of the pancreatic islets (A cells) those of the intestine (EG cells) are completely different. Proper identification of glucagon immunoreactive cells requires the application of morphological and silver staining techniques, at the ultrastructural level.
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PMID:Cytochemical and ultrastructural differentiation of enteroglucagon and pancreatic-type glucagon cells of the gastrointestinal tract. 81 3

The effect of changes in the extracellular redox-state on glucagon-stimulated glucose release by intact isolated rat hepatocytes and the perfused liver was examined. For hepatocytes from the fed rat an increase in pyruvate, ammonium ion or oxygen concentration or a decrease in the lactate/pyruvate or sorbitol/fructose ratios decreased the ability of 1 microM-glucagon to stimulate glucose release without significantly altering the control rate. These changes coincided with a decrease in the lactate/pyruvate ratio of the cell suspension. A decrease in the lactate/pyruvate ratio also decreased the ability of 1 microM-glucagon to stimulate glycogen breakdown measured by loss of contained radioactivity. For the isolated perfused rat liver (fed rat) maximal effects of glucagon as a stimulant of glucose release occurred when lactate instead of pyruvate was present in the perfusion medium. It is concluded that the efficacy of glucagon as a stimulant of glucose release by isolated hepatocytes and the perfused liver depends upon the cytoplasmic redox-state represented by the intracellular lactate/pyruvate ratio.
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PMID:An effect of extracellular redox state on the glucagon-stimulated glucose release by rat hepatocytes and perfused liver. 88 74

The function of clonal insulin-secreting RINm5F cells was compared with parent tumoural B-cells from radiation-induced NEDH rat insulinoma and a RINm5Fr cell line established following transplantation of RINm5F cells in NEDH rat. After 3 days culture, tumoural B-cells contained 156 micrograms insulin/10(6) cells and released 57-82 ng insulin/10(6) cells/h during acute incubations at 2.6 mM Ca2+. RINm5F cells contained 0.56 ng insulin/10(6) cells and released 62-181 pg insulin/10(6) cells/h. Unlike tumoural B-cells, secretion was stimulated 1.7-2.4-fold by 5 mM theophylline, 1 microM glucagon, 25 mM K+, or 7.6 mM Ca2+. Subscapular transplantation of cultured tumoural B-cells or RINm5F cells (2.8 X 10(7) cells/rat) resulted in an encapsulated tumour associated with progressive hyperinsulinaemia, hypoglycaemia and death by 28-46 days and 39-44 days respectively. A RINm5Fr cell line was established in culture from a 19 g tumour 20 days after transplantation. RINm5Fr cells contained 2.69 ng insulin/10(6) cells and released 385-1,017 pg insulin/10(6) cells/h (p less than 0.001 compared with RINm5F cells). Secretion was not augmented by glucose, but at 16.7 mM glucose it was stimulated 1.5-fold by 5 mM theophylline, 1.6-fold by 1 microM glucagon and inhibited 0.6-fold by somatostatin. At 5.6 mM glucose, secretion was stimulated 1.6-fold by 25 mM K+, 2.5-fold by 7.8 mM Ca2+, 2.1-fold by 20 microM A23187, 1.5-fold by 20 mM leucine and 1.4-fold by 100 microM tolbutamide. These data indicate fundamental differences between rat insulinoma cells and the derived RIN cell lines. Transplantation is a useful means to enhance the function of RINm5F cells.
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PMID:Insulin secretion in vivo and in vitro from transplantable NEDH rat insulinoma and derived clonal RINm5F cell line. 282 34

Biological activities of highly potent octapeptide analogs of somatostatin (SS), D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Trp-NH2 (RC-160) and D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Thr-NH2 (RC-121), were investigated in male rats. When analog RC-160 was administered to rats in which serum growth hormone (GH) levels were elevated by pentobarbital anesthesia, a dose-related inhibition of GH was obtained at dose range of 0.1 to 2.5 micrograms/kg. The time course of GH inhibition by RC-160, RC-121 and SS-14 was studied in rats treated with phenobarbital, morphine and chlorpromazine. Analogs RC-160 and RC-121 induced a prolonged inhibition of GH levels, in contrast to SS-14, whose effect was short-lived. The analogs suppressed the GH level for more than 2 hr, the peak inhibition being seen 30 to 60 min after the injection. The effects of analogs RC-160 and RC-121 on insulin secretion were observed in rats, in which insulin levels had been elevated by intravenous administration of glucose (500 mg/rat). Administration of RC-160 suppressed insulin secretion, dose-dependently, maximum but not complete inhibition being achieved at a dose of 100 micrograms/kg. In this model, RC-160 and RC-121, in doses of 30 micrograms/kg, induced a similar inhibition of insulin release as 200 micrograms/kg of SS-14, whose action of SS-14 was transient. The effect of analog RC-160 on glucagon release was studied in rats with glucagon levels elevated by hypoglycemia. RC-160 suppressed the secretion of glucagon, the inhibition being dose-dependent in the range of 0.1 to 2 micrograms/kg. Doses of 2 and 10 micrograms/kg of this analog completely suppressed the hypoglycemia-induced glucagon release. These results indicate that analogs RC-160 and RC-121 possess prolonged and enhanced biological activities, the former analog showing a high selectivity in inhibiting GH and glucagon release in vivo as compared with that of insulin secretion.
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PMID:Effects of highly potent octapeptide analogs of somatostatin on growth hormone, insulin and glucagon release. 288 86

There is increasing evidence that brain cholecystokinin (CCK) peptides function as neuropeptide signals of satiety. Injection of as little as femtomole amounts of CCK-8 into the cerebral ventricles selectively decreased feeding in sheep, and other species (chicken, pig, hamster and rat) also decrease feeding in response to CNS injections of CCK. As would be expected with a physiological satiety agent, CCK-8-induced suppression of feeding interacts in a corrective manner with the energy deficit of the animal, in that the longer the fasting period, the greater the amount of CCK-8 required to suppress feeding. Although it has not been possible to measure changes in concentration of CCK in cerebrospinal fluid (CSF) with feeding, neutralization of endogenous CCK by administration of CCK antisera into the CSF delayed satiety in sheep. This and other evidence not only supports a physiological role for endogenous brain CCK in feeding behavior, but also suggest that CSF transports CCK to site(s) of action. Little is known of CCK's mechanisms of action, but because CNS CCK also causes changes in both gut motility and secretion of insulin and glucagon, the satiety could result directly from effects on behavior, and indirectly through metabolic changes. Evidence of selective uptake of CCK from CSF suggested involvement of hypothalamic periventricular areas in these functions. Recent findings in sheep of a 60% decrease in CCK content in anterior hypothalamus two hrs after a meal also supports this hypothesis.
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PMID:Central nervous system cholecystokinin and the control of feeding behavior in sheep. 300 47

Rat (Rattus norvegicus) and spiny mouse (Acomys cahirinus) are closely related murine species that, due to their altricial (rat) and precocial (spiny mouse) modes of development, differ in the developmental timing of birth. A comparison between the developmental profiles of plasma glucagon, insulin, thyroxine, triiodothyronine, and glucocorticosteroid hormone was carried out to elucidate the question to what extent these hormonal profiles were related to the timing of birth. Although corticosterone is the major circulating glucocorticosteroid in rat, only cortisol was found in the spiny mouse. The onset of increases in glucocorticosteroid and thyroid hormone levels occurred at the same developmental time points in both species. A neonatal increase in triiodothyronine levels was observed in the spiny mouse only. In both species the immediate perinatal period was characterized by decreases in the ratio of insulin and glucagon levels and the level of glucocorticosteroids. The observed developmental patterns of hormonal levels were found to be consistent with the observed developmental pattern of enzymic maturation in the respiratory and gastrointestinal tract, which play a critical role in the adaptation to the extrauterine environment.
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PMID:Hormones in perinatal rat and spiny mouse: relation to altricial and precocial timing of birth. 352 60


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