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)

Somatostatin analogues are potent growth hormone and glucagon inhibitors and are commonly used in the treatment of several endocrine and non-endocrine disorders. We report severe and longstanding hypoglycemia triggered by long-acting octreotide (Sandostatin LAR) in a 62-year-old women with malignant mesenchymal tumor. Hypoglycemia developed after 6 hours of octreotide injection and she was admitted to the emergency unit with sweating, tremor, palpitation and confusion. On admission, her plasma glucose level was: 17 mg/dl (normal: 65-110), cortisol: 31 microg/dl (normal: 5-25), insulin: 4.32 microIU/ml (normal: 6-27), C-peptide: 2.64 ng/ml (normal: 0.9-4.0), growth hormone: 0.06 ng/ml (normal: 0.06-5.0), insulin-like growth factor-I: 8.5 ng/ml (normal: 101-303), insulin-like growth factor binding protein-3: 1715 ng/ml (normal: 2020-3990). Intravenous dextrose infusion was given for a month to sustain normoglycemia since hypoglycemia recurred following cessation of infusion. Therefore, prednisolone, 35 mg/day was added and the parenteral dextrose infusion rate was decreased gradually and finally stopped. Normoglycemia could be maintained with prednisolone 20 mg/day. In patients prone to tumor hypoglycemia, long-acting octreotide may trigger severe and prolonged hypoglycemia due to suppression of counter-regulatory hormones; clinical trial with short-acting octreotide may be warranted to predict and prevent this life-threating complication.
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PMID:Severe and prolonged hypoglycemia triggered by long-acting octreotide in a patient with malignant mesenchymal tumor: case report. 1267 21

Four multiparous lactating cows (175 to 220 d in milk [DIM]) were used in a 4 x 4 Latin square design to assess the effects of four doses (0.0, 0.5, 1.0, and 1.5 microg/kg of body weight) of lipopolysaccharide (LPS; Escherichia coli 0111:B4) on performance and plasma metabolite and hormone concentrations. In addition, effects of immune activation on in vitro hepatic metabolic capacity were evaluated in 12 multiparous lactating cows (150 to 220 DIM) infused with 0 (n = 6), 1.0 (n = 4) or 2.0 (n = 2) microg of LPS/kg. Milk production and DMI decreased linearly with LPS dose for 24 h after LPS infusion. Overall mean plasma tumor necrosis factor-alpha, insulin, glucagon, and cortisol concentrations increased linearly with LPS dose, and plasma beta-hydroxybutyrate decreased linearly by dose after LPS infusion. Infusion of LPS decreased the insulin:glucagon molar ratio, but did not affect plasma concentrations of growth hormone, insulin-like growth factor-1, leptin, or L-(+)-lactate. Plasma concentrations of glucose tended to increase initially and subsequently decrease, and there was a quadratic tendency for increased plasma nonesterified fatty acid concentrations after LPS administration. In vitro hepatic capacity for conversion of [1-(14)C]L-(+)-lactate and [1-(14)C]palmitate, but not [1-(14)C]propionate or [1-(14)C]L-alanine, to CO2 increased after LPS administration. Hepatic capacity to convert [1-(14)C]propionate to glucose tended to increase, but neither esterification nor the conversion of palmitate to acid soluble products was altered by LPS. The LPS infusion resulted in significant changes of endocrine mediators responsible for regulation of energy metabolism of lactating cows and tended to alter subsequent in vitro hepatic metabolic capacity.
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PMID:Effect of lipopolysaccharide on indices of peripheral and hepatic metabolism in lactating cows. 1467 74

Disrupted growth hormone/insulin-like growth factor-1 signaling (DF) and caloric restriction (CR) extend life span and delay the onset of age-related diseases in rodents. In combination, these interventions additively extend life span. To investigate the molecular basis for these effects, we performed genome-wide, microarray expression analysis of liver from homozygous and heterozygous Ames dwarf mice fed ad libitum or CR. CR and DF additively affected a group of 95 genes. Individually and together, DF and CR independently affected the expression of 212 and 77 genes, respectively. These results indicate that DF and CR affect overlapping sets of genes and additively affect a subset of genes. Together, the interventions produced changes in gene expression consistent with increased insulin, glucagon and catecholamine sensitivity, gluconeogenesis, protein turnover, lipid beta-oxidation, apoptosis, and xenobiotic and oxidant metabolism; and decreased cell proliferation, lipid and cholesterol synthesis, and chaperone expression. These data suggest that the additive effects of DF and CR on life span develop from their additive effects on the level of expression of some genes and from their independent effects on other genes. These results provide a novel and focused group of genes closely associated with the regulation of life span in mammals.
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PMID:Additive regulation of hepatic gene expression by dwarfism and caloric restriction. 1503 84

Appropriate insulin therapy is central to the management of all individuals with type 1 diabetes mellitus. The potential role of adjunctive therapy in type 1 diabetes is to improve insulin action, and facilitate the ability of all individuals with type 1 diabetes to achieve and maintain 'better' metabolic control. The landmark clinical trial in type 1 diabetes is the Diabetes Control and Complications Trial (DCCT). The DCCT showed that there is no threshold below which a reduction in glycemia would not provide further benefit against diabetes-related microvascular complications. This study in particular provides the rationale for attempting to achieve as near normoglycemia as possible. We review the use of recognized pharmacologic agents as potential insulin adjunctives in children and adolescents with type 1 diabetes. Adjunctive therapies can be grouped into the following categories based on their putative mechanism of action: enhancement of insulin action (e.g. the biguanides and thiazolidinediones), alteration of gastrointestinal nutrient delivery (e.g. acarbose and amylin), and other targets of action (e.g. pirenzepine and insulin-like growth factor-1 [IGF-1], which reduce growth hormone secretion, and glucagon-like peptide-1, which acts to stimulate insulin secretion). Many of these agents have been found to be effective in short-term studies with decreases in glycosylated hemoglobin of 0.5-1.0%, lowered postprandial blood glucose levels, and decreased daily insulin doses. Adverse effects such as poor gastrointestinal tolerability (metformin, acarbose) or potential acceleration of retinopathy (IGF-1) indicates the need for further studies of efficacy, safety, and patient selection before these adjunctive therapies can be widely recommended in type 1 diabetes.
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PMID:Potential adjunctive therapies in adolescents with type 1 diabetes mellitus. 1551 Nov 28

Insulin-like growth factor-1 (IGF-1) functions as a growth factor regarding physiological regulations of cellular metabolism, regeneration and growth. In pancreas islets their potential function is unclear and only little information is available on occurrence and distribution of the corresponding insulin-like growth factor-1 receptor (IGF-1R) in islet cells. Therefore, we investigated the localization of IGF-1R by immunohistochemical techniques and its possible co-localization with other islet hormones. Further, we applied molecular biology techniques to determine the present of local gene expression of IGF-1R and IGF-1. Immunostaining on serial sections with anti-insulin, anti-glucagon and anti-somatostatin antibodies shows, IGF-1R was selectively expressed in insulin-producing B-cells and additionally more pronounced in somatostatin-containing D-cells, which are located in the periphery of porcine pancreatic islets. Furthermore, the RT-PCR experiment demonstrates clearly that IGF-1 and IGF-1R was expressed together in the porcine pancreas. The high expression of IGF-1R in porcine D-cells indicates that mammalian IGF-1R genes are regulated in a different manner since it was shown that in all other species IGF-1R was expressed in B- and A-cells but not in D-cells.
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PMID:Cell-type specific expression of IGF-1R in porcine islet cells. 1570 70

The growth arrest after hypophysectomy in rats is mainly due to growth hormone (GH) deficiency because replacement of GH or insulin-like growth factor (IGF) I, the mediator of GH action, leads to resumption of growth despite the lack of other pituitary hormones. Hypophysectomized (hypox) rats have, therefore, often been used to study metabolic consequences of GH deficiency and its effects on tissues concerned with growth. The present study was undertaken to assess the effects of hypophysectomy on the serum and pancreatic levels of the three major islet hormones insulin, glucagon, and somatostatin, as well as on IGF-I. Immunohistochemistry (IHC), in situ hybridization (ISH), radioimmunoassays (RIA), and Northern blot analysis were used to localize and quantify the hormones in the pancreas at the peptide and mRNA levels. IHC showed slightly decreased insulin levels in the beta cells of hypox compared with normal, age-matched rats whereas glucagon in alpha cells and somatostatin in delta cells showed increase. IGF-I, which localized to alpha cells, showed decrease. ISH detected a slightly higher expression of insulin mRNA and markedly stronger signals for glucagon and somatostatin mRNA in the islets of hypox rats. Serum glucose concentrations did not differ between the two groups although serum insulin and C-peptide were lower and serum glucagon was higher in the hypox animals. These changes were accompanied by a more than tenfold drop in serum IGF-I. The pancreatic insulin content per gram of tissue was not significantly different in hypox and normal rats. Pancreatic glucagon and somatostatin per gram of tissue were higher in the hypox animals. The pancreatic IGF-I content of hypox rats was significantly reduced. Northern blot analysis gave a 2.6-, 4.5-, and 2.2-fold increase in pancreatic insulin, glucagon, and somatostatin mRNA levels, respectively, in hypox rats, and a 2.3-fold decrease in IGF-I mRNA levels. Our results show that the fall of serum IGF-I after hypophysectomy is accompanied by a decrease in pancreatic IGF-I peptide and mRNA but by partly discordant changes in the serum concentrations of insulin and glucagon and the islet peptide and/or mRNA content of the three major islet hormones. It appears that GH deficiency resulting in a "low IGF-I state" affects translational efficiency of these hormones as well as their secretory responses. The maintenance of normoglycemia in the presence of reduced insulin and elevated glucagon serum levels, both of which would be expected to raise blood glucose, may result mainly from the enhanced insulin sensitivity, possibly due to GH deficiency and the subsequent decrease in IGF-I production.
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PMID:The effect of hypophysectomy on pancreatic islet hormone and insulin-like growth factor I content and mRNA expression in rat. 1581 46

Plant proteins have a reduced content of essential amino acids in comparison to animal proteins. A significant reduction of limiting amino acids (methionine, lysine, tryptophan) means lower protein synthesis. In subjects with predominant or exclusive consumption of plant food a higher incidence of hypoproteinemia due to significant reduction of methionine and lysine intakes was observed. On the other hand, lower intake of these amino acids provides a preventive effect against cardiovascular disease via cholesterol regulation by an inhibited hepatic phospholipid metabolism. Vegetarians have a significantly higher intake of non-essential amino acids arginine and pyruvigenic amino acids glycine, alanine, serine. When plant protein is high in non-essential amino acids, down-regulation of insulin and up-regulation of glucagon is a logical consequence. The action of glucagon in the liver is mediated by stimulation of adenyl cyclase that raises cyclic-AMP (adenosine-3,5-monophosphate) concentrations. Cyclic-AMP down-regulates the synthesis of a number of enzymes required for de novo lipogenesis and cholesterol synthesis, up-regulates key gluconeogenic enzymes and the LDL receptors and decreases the IGF-1 activity (insulin-like growth factor). Cyclic-AMP thus provides a reduction of atherosclerosis risk factors as well as a retardation of cancer development. A sufficient consumption of plant proteins has the protective effects against chronic degenerative diseases (Tab. 2, Ref. 26).
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PMID:Health benefits and risks of plant proteins. 1620 43

Glucagon-expressing retinal amacrine cells have been implicated in regulating postnatal ocular growth. Furthermore, experimentally accelerated rates of ocular growth increase the number of neurons added to the peripheral edge of the retina. Accordingly, we assayed whether glucagon-expressing neurons within the retina regulate the proliferation of progenitors in the circumferential marginal zone (CMZ) of the postnatal chicken eye. We found that glucagon-containing neurites are heavily clustered within the CMZ at the peripheral edge of the retina. Many of these neurites originate from a cell type that is distinct from other types of retinal neurons, which we termed large glucagon-expressing neurons (LGENs). The LGENs are immunoreactive for glucagon and glucagon-like peptide 1 (GLP1), have a unipolar morphology, produce an axon that projects into the CMZ, and are found only in ventral regions of the retina. In dorsal regions of the retina, a smaller version of the LGENs densely ramifies neurites in the CMZ. Intraocular injections of glucagon or GLP1 suppressed the proliferation of progenitors in the CMZ, whereas a glucagon-receptor antagonist promoted proliferation. In addition, we found that glucagon, GLP1, and glucagon antagonist influenced the number of progenitors in the CMZ. We conclude that the LGENs may convey visual information to the CMZ to control the addition of new cells to the edge of the retina. We propose that glucagon/GLP1 released from LGENs acts in opposition to insulin (or insulin-like growth factor) to regulate precisely the proliferation of retinal progenitors in the CMZ.
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PMID:Glucagon-expressing neurons within the retina regulate the proliferation of neural progenitors in the circumferential marginal zone of the avian eye. 1626 23

Of the U.S. population, 65% is either overweight or obese, and weight loss is recommended to reduce co-morbid conditions. However, bone mobilization and loss may also occur with weight loss. The risk for bone loss depends on initial body weight, age, gender, physical activity, and conditions of dieting such as the extent of energy restriction and specific levels of nutrient intake. Older populations are more prone to bone loss with weight loss; in women, this is due at least in part to a reduced dietary Ca intake and/or efficiency of absorption. Potential hormonal mechanisms regulating bone loss during weight loss are discussed, including decreases in estrogen, leptin, glucagon-like peptide-2, growth hormone, and insulin-like growth factor-1, or an increase in cortisol. In contrast, the rise in adiponectin and ghrelin with weight reduction should not be detrimental to bone. Combining energy restriction with exercise does not necessarily prevent bone loss, but may attenuate loss as was shown with additional Ca intake or osteoporosis medications. Future controlled weight loss trials should be designed to further address mechanisms influencing the density and quality of bone sites vulnerable to fracture, in the prevention of osteoporosis.
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PMID:Bone, body weight, and weight reduction: what are the concerns? 1670 2

A 54-year-old man with a past history of multi-operation for solitary fibrous tumor was hospitalized for hypoglycemia. Computed tomography demonstrated multiple tumors in the liver but not in the pancreas. His serum insulin-like growth factor (IGF)-II level was normal, but immunoblot analysis and immunohistochemistry revealed a high molecular weight form of IGF-II in the serum and tumor. Surgical resection was impossible, because of tumor dissemination. Hypoglycemia was repeated despite infusion of glucose and glucagon. Glucocorticoid dramatically and continuously abolished hypoglycemia. In cases of inoperable IGF-II-producing tumor, glucocorticoid therapy may be promising for hypoglycemia.
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PMID:Glucocorticoid therapy ameliorated hypoglycemia in insulin-like growth factor-II-producing solitary fibrous tumor. 1670 45


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