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)

Thus far, somatostatin has been used primarily as a research tool to investigate pancreatic alpha- and beta- cell function. On the basis of its ability to inhibit insulin and glucagon secretion, several therapeutic applications have been suggested: e.g., as an adjunct in the treatment of diabetes mellitus, or as a palliative agent in inoperable islet tumors. Current experiments are underway to develop more specific analogs with longer durations of action to permit clinical evaluation of these potential applications. The presence of somatostatin within the pancreatic D cells raises the possibility that it may function as a local regulator of insulin and glucagon release. Clearly, further work is needed to delineate the factors governing the secretion of somatostatin and its mode of action. Such studies may uncover a new class of syndromes resulting from D-cell dysfunction.
Curr Top Mol Endocrinol 1976
PMID:Somatostatin and the endocrine pancreas. 21 Oct 5

1. Studies were performed to investigate the metabolic fate of dipeptides when administered intravenously in rats. Glycyl-leucine, glycylglycine or glycylsarcosine was injected into the jugular vein. The plasma disappearance rate after the peak plasma concentrations was most rapid for glycyl-leucine and least rapid for glycylsarcosine. 2. During urine collection for 40 min, trace amounts of glycyl-leucine and glycylglycine and 13% of the injected glycylsarcosine were excreted. 3. Neither glycylglycine nor glycyl-leucine was detected in the liver, muscle, intestinal mucosa or renal cortex, but concentrations of glycine or leucine, or both, in these tissues were increased after each injection. In contrast, glycylsarcosine was recovered in all these tissues with concentrations in the renal cortex being far greater than in any other tissue, but sarcosine was found only in the renal cortex and intestinal mucosa. 4. The changes in plasma concentrations of free amino acids, glucose and glucagon, and tissue concentrations of free amino acids, were similar after the intravenous administration of glycyl-leucine and an equimolar mixture of free glycine and leucine. However, the amount of insulin secreted during the 40 min after glycyl-leucine injection was 1-6 times that produced after the injection of the corresponding amino acid mixture. 5. Results show that, within the present experimental conditions, the intravenous administration of dipeptides is as effective as that of the corresponding free amino acids in enriching the tissue pools of amino acids. It is suggested that efficient hydrolysis by cellular enzymes prohibits accumulation of intact dipeptides in body tissues.
Clin Sci Mol Med 1977 Feb
PMID:Metabolism of intravenously administered dipeptides in rats: effects on amino acid pools, glucose concentration and insulin and glucagon secretion. 40 46

Synthesis of malic enzyme was rapidly and markedly stimulated by the addition of triiodothyronine to chick embryo liver cells in culture. Alpha-Amanitin, an inhibitor of DNA-dependent RNA polymerase II, blocked induction. The kinetics of induction and de-induction of malic enzyme synthesis suggested that the most stable event in triiodothyronine induction had a half-life of 18 to 20 h. However, malic enzyme synthesis decayed with a half-life of 2,4 h when transcription was inhibited with alpha-amanitin. Thus a long-lived event in thyroid hormone stimulation of malic enzyme synthesis occurred prior to transcription of a specific messenger RNA (mRNA), presumably malic enzyme mRNA. Malic enzyme synthesis decayed with a half-life of about 2 h when glucagon was added to pre-induced liver cells. The similarity of decay rates after inhibition of transcription with alpha-amanitin or inhibition of malic enzyme synthesis by glucagon suggests that glucagon may inhibit the transcription or processing of a specific mRNA required for malic enzyme synthesis.
Mol Cell Endocrinol 1978 Jun
PMID:Regulation of malic enzyme synthesis by thyroid hormone and glucagon: inhibitor and kinetic experiments. 56 41

1. Infusion of a triglyceride emulsion (Intralipid) into overnight fasted normal subjects produced a rise in plasma free fatty acids (FFA) and blood ketones. 2. Glucose given orally 60 min after the start of the Intralipid infusion produced a sharp fall in blood ketones without much change in plasma FFA. 3. An infusion of glucagon given together with Intralipid did not alter the reduction in blood ketones produced by oral glucose in normal subjects. 4. Oral glucose given 60 min after the start of the Intralipid infusion in three insulin-requiring diabetic subjects produced no fall in blood ketones. 5. The results suggest that glucose prevents the increase in blood ketones after Intralipid through an increase in insulin secretion rather than through a suppression of glucagon or as a direct effect of glucose. 6. It is most likely that the effect of insulin is to inhibit hepatic ketogenesis.
Clin Sci Mol Med 1978 Nov
PMID:Evidence for an hepatic anti-ketogenic effect of insulin in man. 72 4

Gluconeogenesis by isolated hepatocytes resulted in glucose release but insignificant rates of glycogen synthesis. The effectiveness of precursors was similar for hepatocytes from fed and starved chickens except for impaired gluconeogenesis from pyruvate when compared to lactate in lactate starved chicken hepatocytes. The impairment was caused by limitations in cytosolic NADH production as a result of the mitochondrial location of phosphoenolpyruvate carboxykinase in chicken liver. The order of effectiveness of precursors on hepatic gluconeogenesis was generally similar to the effects of precursors on increasing the plasma glucose concentration in vivo. The exceptions were caused by interactions with other precursors in vivo. The alteration of the NADH/NAD+ ratio by ethanol and ATP/ADP ratio by adenosine could play significant roles in the control of precursor conversion to glucose. Physiological glucagon concentrations stimulated gluconeogenesis from precursors entering the pathway both above and below the level of triose phosphates, and its effect were mimicked by dibutyryl cyclic AMP. Previous results on the effects of precursor and glucagon injection on the plasma glucose concentration of chickens in vivo can largely be explained by effects at the hepatic level. Isolated chicken and rat hepatocytes share many common features. Qualitatively the ordering of gluconeogenic effectiveness was similar but quantitive differences existed as a result of differing activities and cellular locations of enzymes. Neither preparation readily synthesised glycogen and the sensitivity to glucagon was similar.
Mol Cell Biochem 1978 Dec 22
PMID:Hepatic gluconeogenesis in chickens. 74 98

Determinations of the calcium pools in myocardial cells in vitro have shown the existence of at least three pools of exchangeable calcium. Epinephrine and glucagon were found to produce significant increases in the size of the two slower exchanging pools. Prostaglandins E1 and F1alpha also increased significantly calcium pool size whereas E2 and F2alpha did not; results which correlate well with the effects of the two former prostaglandins on intracellular cAMP levels. The results imply that these agents cause small, but significant, changes in the transmembrane exchange of calcium and large increases in the intracellular calcium pool. Effects which may involve the direct or indirect action of cAMP.
Mol Cell Endocrinol 1976 Oct
PMID:The effects of hormones and prostaglandins on the calcium pools in cultured myocardial cells. 97 90

1. The effect of calcitonin, a large amount of calcium given orally, pentagastrin and glucagon on plasma 47Ca radioactivity curves in subjects pretreated with 47Ca was examined. 2. A sudden increase of plasma radioactivity after intravenous administration of calcitonin and pentagastrin and after the oral calcium load was observed in normal subjects; the intravenous infusion of glucagon was less effective. 3. Two thyroparathyroidectomized patients who responded to the calcitonin infusion did not respond to the oral calcium load. 4. These data may be considered to offer indirect evidence of endogenous calcitonin secretion in man.
Clin Sci Mol Med 1976 Sep
PMID:Indirect evidence of calcitonin secretion in man. 98 25

By measuring the specific radioactivity of glucose released from isolated perfused livers of normal, fed rats in the presence of [U-14C]fructose, the gluconeogenetic and glycogenolytic contributions to glucose production were estimated. After 20 min of perfusion with 4 mM fructose, glycogenolysis was inhibited by 40% in the absence and by 70% in the presence of glucagon (3 nM). Glucagon decreased the release of lactate plus pyruvate and enhanced glucose formation from fructose without affecting its uptake. Glycerol (4 mM) and xylitol (3 mM) had qualitatively similar, but smaller effects on glucagon-stimulated glycogenolysis. The glucagon-mediated phosphorylase b to a conversion was not altered by fructose, indicating that glycogenolysis was decreased as a consequence of an inhibition of phosphorylase a. During the first minutes after the addition of fructose, decreased ATP/AMP ratios and tissue Pi levels correlated with a transient increase of phosphorylase a activity. It was concluded that the effects of fructose on the control of hepatic glycogenolysis and glucose production were the result of a complex interplay between a transient b to a conversion of phosphorylase and an inhibition of the a-form of the enzyme, possibly by fructose 1-phosphate and other phosphorylated metabolites.
Mol Cell Endocrinol 1976 Nov
PMID:Interactions of glucagon and fructose in the control of glycogenolysis in perfused rat liver. 100 7

1. The effects of lanthanum on renin release and renal vasoconstriction were studied in the isolated perfused rat kidney. 2. Lanthanum reduced noradrenaline-induced renal vasoconstriction. 3. Lanthanum prevented isoprenaline-induced and glucagon-induced stimulation of renin secretion.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Blockade of renin release by lanthanum. 107 84

The number and coupling efficiency of beta-adrenoceptors in liver membranes and intact hepatocytes of lactating and non-lactating female rats were compared to assess whether or not alterations in this signalling system could contribute towards the changed pattern of hepatic metabolism during lactation. In view of the different adaptations of hepatic metabolism to lactation in ruminants, the adrenergic receptor profile of sheep liver membranes was also determined. Post-receptor responses at two stages 'down-stream' of cyclic AMP generation were also evaluated in rat hepatocytes in response to the beta-adrenergic agonist isoprenaline. No changes in the number of affinity of hepatic beta-adrenoceptors were found in sheep or rats when lactating and non-lactating individuals were compared. Sheep liver was found to have a much greater concentration of beta-adrenoceptors than rat liver, and a much higher ratio of beta:alpha 1. The sensitivity and responsiveness of cyclic AMP generation in response to isoprenaline were similar in hepatocytes prepared from lactating and non-lactating rats, although the response to saturating concentrations of glucagon was diminished in hepatocytes from lactating rats. The activity ratio of cyclic AMP-dependent protein kinase (PK-A) also reacted similarly (in respect of both responsiveness and sensitivity) to isoprenaline in these two groups of hepatocytes. Contrastingly, the sensitivity of rat hepatocyte phosphorylase activity to beta-adrenergic stimulation was greatly diminished during lactation.
Mol Cell Biochem 1992 Nov 04
PMID:Effects of lactation on the regulation of hepatic metabolism in the rat and sheep: adrenergic receptors and cyclic AMP responses. 133 22


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