Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Previous studies demonstrated that insulin-induced hypoglycemia enhances glicentin secretion in piglets and prompted us to investigate the response of glucagon-like immunoreactivity (GLI) to hypoglycemia in dogs. Insulin hypoglycemia did not induce any rise of plasma total immunoreactive glucagon (IRG) measured by nonspecific antiserum to glucagon in normal or pancreatectomized dogs under anesthesia. In contrast, insulin-induced hypoglycemia clearly increased plasma total IRG in both normal and pancreatectomized dogs in a conscious state. Administration of acetylcholine resulted in an elevation of plasma total IRG, whereas epinephrine induced a slight increase in plasma total IRG. The infusion of alpha- or beta-adrenergic blockers did not affect the response of plasma total IRG to hypoglycemia, whereas atropine completely blunted the increase in plasma total IRG during insulin hypoglycemia. Similarly atropine abolished the rise of plasma total IRG during intravenous administration of 2-deoxy-D-glucose. It is concluded that hypoglycemia clearly enhances the secretion of GLI from the gut in dogs and that GLI secretion during hypoglycemia is modulated, at least in part, by the autonomic nervous system.
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PMID:Response of gut glucagon-like immunoreactivity to hypoglycemia in dogs. 264 47

The phospho-oligosaccharide extracted from rat liver and supposed to act as the insulin second messenger inhibits glucose-stimulated insulin release. In the present study, this phospho-oligosaccharide was found not to affect D-[U-14C]glucose oxidation and 45Ca net uptake, but to inhibit insulin release evoked by either D-glucose or 2-ketoisocaproate in isolated rat islets. The relative extent of the latter inhibition was unaffected by either the concentration of D-glucose or the presence of dibutyryl-cyclic AMP, forskolin or glucagon in the incubation medium. At variance with the inhibitory effect of clonidine, that of the phospho-oligosaccharide was resistant to both blockade of alpha 2-adrenergic receptors or pre-treatment with the toxin of Bordetella pertussis. It is speculated, therefore, that such a phospho-oligosaccharide might interfere with a distal event in the insulin secretory sequence.
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PMID:Effect of a phospho-oligosaccharidic putative insulin messenger on insulin release in rats. 266 15

Rat pancreatic beta cells were transformed by simian virus 40 (SV40). The established beta cell lines expressed tumor antigen specific to SV40 and retained the ability to produce immunoreactive insulin (IRI) even at a high passage level. One of 12 transformed beta cell lines, SV-PB1205, was further investigated in vitro and in vivo. Firstly, effects of drugs on replication of the pancreatic beta cells were examined in in vitro experiments. Various drugs increased the uptake of 3H-thymidine into the cells. Those included D-glucose, tetragastrin and secretin. However, such effect was not observed for glucagon and growth hormone. Secondly, the SV40-transformed pancreatic beta cells were transplanted into diabetic rats. This produced such improvement of plasma glucose level at least for 2 weeks. The Significance of those experiments was discussed.
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PMID:Establishment and characterization of rat pancreatic beta cell lines transformed by simian virus 40. 283 40

Secretin and glucagon potentiate glucose-induced insulin release. We have compared the effects of secretin and glucagon with that of four hybrid molecules of the two hormones on insulin release and formation of cyclic AMP (cAMP) in isolated mouse pancreatic islets. All six peptides potentiated the release of insulin at 10 mM D-glucose, and their effects were indistinguishable with respect to the dynamics of release, dose-response relationship, and glucose dependency. However, measurements of cAMP accumulation in the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (10(-4) M) showed that the fold increase compared with glucose alone had the following ranking order: secretin = [Tyr10, Tyr13]-secretin 1.6 less than [Tyr10, Tyr13, Trp25]secretin 1.8 less than glucagon 1.9 less than [Asp3, Glu9, Arg12]glucagon 2.3 = [Asp3, Glu9]glucagon. These results suggest that despite similar potentiating effects of secretin and glucagon on glucose-induced insulin release, their modes of action may be different.
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PMID:Insulin release by glucagon and secretin: studies with secretin-glucagon hybrids. 283 12

Neuroglucopenia (NGP), which is a serious potential hazard for all insulin-treated diabetics, stimulates many neural and hormonal responses including increased glucagon secretion and activation of beta-adrenergic receptors of the autonomic nervous system. To determine which of these responses is important in recovery from NGP, we induced NGP in baboons by the intravenous (IV) injection of 2-deoxy-D-glucose with and without beta-adrenergic blockade (propranolol) and somatostatin. Thirty minutes after the induction of NGP the animals recovered, and the mean (+/- SEM) rise in arterial plasma glucose was 6.6 +/- 0.9 mmol/L, in glycerol 0.106 +/- 0.22 mmol/L, and in beta-hydroxybutyrate 0.091 +/- 0.22 mmol/L. Animal recovery and glucose rise were uninfluenced by the infusion of propranolol (mean 30 minute plasma glucose rise of 6.2 +/- 0.8 mmol/L) and somatostatin (6.8 +/- 0.8 mmol/L). However, the combined infusion of somatostatin and propranolol prevented animal recovery and glucose rise (1.0 +/- 0.1 mmol/L). The glycerol and beta-hydroxybutyrate rises were blocked by the propranolol infusion alone. Thus, recovery from NGP and the associated rise in plasma glucose, glycerol, and beta-hydroxybutyrate are prevented by the combination of the suppression of the glucagon and beta-adrenergic response to NGP. Furthermore, if the results of our study are extrapolated to insulin-dependent diabetic patients, most of whom have an impaired glucagon response to insulin-induced hypoglycemia/neuroglucopenia, they would be critically dependent on beta-adrenergic mechanisms for recovery from NGP.
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PMID:Glucose counterregulation during recovery from neuroglucopenia: which mechanism is important? 285 49

We investigated the effect of several potential carbohydrate secretagogues, amino acids, a ketoacid, and potassium chloride on insulin, glucagon, and somatostatin release from the in vitro perfused Brockmann body of channel catfish (Ictalurus punctatus). Mannose (15 mM) stimulated the release of insulin and somatostatin. Fructose (30 mM) induced only a small and transient release of somatostatin. Galactose (15 mM) was not a secretagogue. Likewise, glyceraldehyde failed to stimulate hormone release. Among the amino acids newly tested, alanine and leucine, and also alpha-ketoisocaproic acid were without effect. A high concentration of potassium (25 mEq/liter) induced a pronounced release of insulin and glucagon and a moderate release of somatostatin. In conclusion, a striking similarity exists between catfish and higher vertebrates in their pancreatic endocrine response to hexoses; on the other hand, the catfish Brockmann body appears to respond only to a few of the common stimuli of pancreatic hormone release in mammals.
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PMID:Secretagogues for pancreatic hormone release in the channel catfish (Ictalurus punctatus). 288 40

Neonatal mice, under fasting conditions, are susceptible to the development of lesions in the arcuate nucleus (AN) of the hypothalamus, with high doses of monosodium L-glutamate (MSG). Feeding of nutrients (e.g., sugars and L-amino acids) has been shown to have a protective effect against the development of these lesions. The purpose of these studies was to elucidate the mechanism of this protective effect. Histopathologic examination of lesions of the AN demonstrated that feeding of weaning mice before subcutaneous administration of toxic doses of MSG suppressed the development of these lesions, as compared to fasted controls. Similarly, the number of necrotic cells in the AN of neonates administered toxic doses of MSG subcutaneously was reduced when D-glucose and L-arginine were administered orally. Atropine obliterated the protective effect of D-glucose. Pretreatments consisting of gastric inhibitory polypeptide (GIP) + oral D-glucose had a protective effect of higher potency than GIP alone. Pretreatments with insulin, anorexigenic peptide (pyroGlu-His-Gly), cholecystokinin, glucagon, bombesin, and substance P (in decreasing order of effectiveness) demonstrated a protective effect against the AN lesion in neonates, whereas somatostatin and beta-endorphin had no effect. Results suggest that the protective effect of nutrients may in part be due to the stimulation of peptide hormone release during the postabsorptive phase. It is postulated that the effect of entero-pancreatic hormone, especially insulin, is to enhance the tolerance of AN neurons of neonatal mice to the toxic dose of L-glutamate.
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PMID:Mealing and related hormone release suppress hypothalamic lesions of neonatal mice by L-glutamate. 288 96

Intercellular communication via gap junctions, as measured by dye and electrical coupling, disappears within 12 h in primary rat hepatocytes cultured in serum-supplemented media or within 24 h in cells in a serum-free, hormonally defined medium (HDM) designed for hepatocytes. Glucagon and linoleic acid/BSA were the primary factors in the HDM responsible for the extended life span of the electrical coupling. After 24 h of culture, no hormone or growth factor tested could restore the expression of gap junctions. After 4-5 d of culture, the incidence of coupling was undetectable in a serum-supplemented medium and was only 4-5% in HDM alone. However, treatment with glycosaminoglycans or proteoglycans of 24-h cultures, having no detectable gap junction protein, resulted in synthesis of gap junction protein and of reexpression of electrical and dye coupling within 48 h. Most glycosaminoglycans were inactive (heparan sulfates, chondroitin-6 sulfates) or only weakly active (dermatan sulfates, chondroitin 4-sulfates, hyaluronates), the weakly active group increasing the incidence of coupling to 10-30% with the addition of 50-100 micrograms/ml of the factor. Treatment of the cells with 50-100 micrograms/ml of heparins derived from lung or intestine resulted in cells with intermediate levels of coupling (30-50%). By contrast, 10-20 micrograms/ml of chondroitin sulfate proteoglycan, dermatan sulfate proteoglycan, or liver-derived heparin resulted in dye coupling in 80-100% of the cells, with numerous cells showing dye spread from a single injected cell. Sulfated polysaccharides of glucose (dextran sulfates) or of galactose (carrageenans) were inactive or only weakly active except for lambda-carrageenan, which induced up to 70% coupling (albeit no multiple coupling in the cultures). The abundance of mRNA (Northern blots) encoding gap junction protein and the amounts of the 27-kD gap junction polypeptide (Western blots) correlated with the degree of electrical and dye coupling indicating that the active glycosaminoglycans and proteoglycans are inducing synthesis and expression of gap junctions. Thus, proteoglycans and glycosaminoglycans, especially those found in abundance in the extracellular matrix of liver cells, are important in the regulation of expression of gap junctions and, thereby, in the regulation of intercellular communication in the liver. The relative potencies of heparins from different tissue sources at inducing gap junction expression are suggestive of functional tissue specificity for these glycosaminoglycans.
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PMID:Proteoglycans and glycosaminoglycans induce gap junction synthesis and function in primary liver cultures. 288 11

Four infants (three boys and one girl, ages 12-89 days) with persistent hyperinsulinism secondary to nesidioblastosis (two) or microadenoma of the pancreas (two) were treated with cyclic somatostatin (S) as part of the preoperative management until subtotal pancreatectomy was performed within 12 to 35 days. The individual dose dependent response of glucoregulatory hormones to exogenous was evaluated by means of the "somatostatin sensitivity test" (SST). Thereby S was infused in stepwise increasing doses, as dictated by the prevailing blood glucose levels, until normoglycemia was achieved concomitantly with a dextrose infusion at rates of 5 mg/kg/min. This procedure resulted only in a partial suppression of insulin, C-peptide, glucagon, HGH and cortisol, without recurrence of hypoglycemia. Compared to baseline levels, plasma concentrations of insulin decreased by 61%, of C-peptide by 64% and a rise of glucagon by 23% was observed. The SST which can be performed under routine clinical conditions, is a useful procedure for evaluating the individual S-dose necessary to achieve normoglycemia. The risk of total S-induced suppression of hormones, such as IRI, IRCP, HGH, glucagon and cortisol can be omitted.
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PMID:[Preoperative management of newborn infants with hyperinsulinemic hypoglycemia (2)]. 289 Jul 92

In isolated perfused rat pancreases, the alpha-anomer of D-glucose is more potent than beta-D-glucose not solely in stimulating insulin release and suppressing glucagon output, but also in causing somatostatin secretion.
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PMID:Anomeric specificity of glucose-induced somatostatin secretion. 289 61


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