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)

Chronic portal hypertension is associated with systemic hypotension and reduced peripheral vascular resistance. Although it is well established that splanchnic and renal vascular resistances are reduced, the contribution of possible alterations in skeletal muscle hemodynamics in portal hypertension is unknown. The present study was designed to determine if skeletal muscle vascular resistance was reduced and blood flow increased in portal hypertensive rats. In portal hypertensive animals, hind-quarter blood flow was significantly increased while vascular resistance was significantly reduced. The fall in resistance in the portal hypertensive animals was associated with an increase in the capillary filtration coefficient, suggesting that an increase in functional exchange vessel surface area occurred. Cross perfusion of control hindquarters with portal hypertensive blood resulted in a 38% reduction in hindquarter vascular resistance. Raising the plasma glucagon concentration to levels reported in portal hypertensive animals resulted in no change in blood flow or vascular resistance in control hindquarters. Skeletal muscle vascular sensitivity to norepinephrine was assessed by constructing dose-response curves in control and portal hypertensive animals. Mean ED50 values were not different. The results of these studies indicate that skeletal muscle vascular resistance is reduced in portal hypertension and humoral factors, but not glucagon, are primarily responsible for the skeletal muscle hyperemia associated with portal hypertension.
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PMID:Humoral factors may mediate increased rat hindquarter blood flow in portal hypertension. 405 Oct 18

In patients with portal hypertension, plasma insulin levels were raised both fasting and after oral glucose or intravenous tolbutamide. This supports previous suggestions that resistance to endogenous insulin plays a major role in producing the impaired glucose tolerance found in chronic hepatic dysfunction. The operation of portacaval anastomosis was followed by impaired oral fructose tolerance, but did not significantly change oral glucose tolerance. Plasma insulin levels were unchanged by the operation, either fasting or following the stimulus of an oral glucose load or intravenous tolbutamide. The insulin response after operation was only higher after intensive pancreatic beta cell stimulation by a combination of glucose, tolbutamide, and glucagon. These results indicate that, in patients with hepatic dysfunction, little insulin is being removed by the liver from the portal blood except when the insulin secretory rate is unusually high.
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PMID:The effect of portacaval anastomosis on oral carbohydrate tolerance and on plasma insulin levels. 506 Jun 71

Plasma level of immunoreactive insulin (IRI) and C-peptide (CPR), and their responses to intravenous administration of glucagon were studied in 37 patients with cirrhotic portal hypertension during hepatic vein catheterization. IRI and CPR in peripheral vein and hepatic vein were compared with development of portal vein collaterals measured by indocyanine green disappearance tests and portal venograms. In additional 2 cases, the values were compared with those of portal vein blood obtained by percutaneous transhepatic catheterization. Plasma IRI of peripheral vein in cirrhotic patients, those who had only esophageal varices but did not have remarkable amount of portal vein collateral blood flow, revealed the changes closely resembling the controls. On the contrary, peripheral vein IRI elevated significantly in cirrhotics with large shunt and the values exceeded those of hepatic vein, although responses to the glucagon test were normal. In experimental study using dogs, peripheral IRI revealed significant increase after the portocaval anastomosis diverting the portal blood containing high IRI into the inferior vena cava, and the values exceeded those of hepatic vein. It is important to know the development of portal vein collaterals as a major cause of hyperinsulinemia in liver cirrhosis.
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PMID:[Clinical and experimental studies on elevated plasma level of insulin in cirrhotic patients with portal hypertension and portosystemic collateral circulation]. 637 13

The role of neural, metabolic, physical, and humoral factors in the intestinal hyperemia associated with chronic portal hypertension was examined by use of the rat portal vein stenosis model. Intestinal blood flow and splenic pulp pressure were increased, while systemic arterial pressure and total vascular resistance were reduced in portal vein-stenosed rats as compared with controls. The reduction in total vascular resistance was entirely due to a fall in precapillary resistance and was accompanied by an increase in intestinal capillary pressure, which exceeded that produced by acute portal pressure elevation to the same level. Arteriovenous shunting of 15-micron microspheres was four times higher in portal-hypertensive rats. Cross-perfusion of control intestinal preparations with arterial blood from portal-hypertensive rats produced a 30% increase in blood flow. Plasma glucagon levels in portal-hypertensive rats were three times higher than in controls. Intra-arterial infusion of glucagon (at a rate that achieved the concentration measured in portal-hypertensive animals) produced a 20% reduction in intestinal vascular resistance. The results of these studies indicate that humoral factors, including glucagon, are primarily responsible for the hyperemia associated with portal hypertension.
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PMID:Role of humoral factors in the intestinal hyperemia associated with chronic portal hypertension. 649 39

The finding of high plasma free fatty acid (FFA) levels in cirrhotic patients has been attributed either to decreased hepatic clearance or to enhanced fat mobilization. To better clarify these hypotheses, total and individual FFA and glycerol levels were determined in 21 cirrhotic patients with different degrees of hepatocellular damage (evaluated by liver function tests), portal hypertension (evaluated by endoscopy and clinical signs), and nutritional status (evaluated by anthropometric and biohumoral parameters) and in 10 age- and sex-matched healthy subjects. Glucose tolerance and insulin and glucagon levels were determined in all individuals. Well-nourished and malnourished patients were identified within the cirrhotic group. Plasma FFA and glycerol concentrations were well correlated (r = 0.47, P less than 0.05), levels being significantly higher in cirrhotic individuals than in controls (746.6 +/- 46.29 SE v 359.22 +/- 40.82 mumol/L, P less than 0.001 for plasma FFA; 150.1 +/- 3.12 v 82.5 +/- 9.2 mumol/L, P less than 0.01 for glycerol). Plasma FFA and glycerol showed no correlation with the liver function test results or portal hypertension parameters. Interestingly, plasma levels of FFA and glycerol were influenced by the nutritional status, significantly higher FFA levels being observed in the well-nourished than in the malnourished patients (842.5 +/- 47.5 v 563.4 +/- 78 mumol/L, P less than 0.005). Furthermore, a positive correlation was found between plasma glycerol level and percentage of triceps skinfold (r = 0.45, P less than 0.05). No correlation was found between plasma levels of FFA or glycerol and glucose tolerance, insulin and glucagon.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Total and individual free fatty acid concentrations in liver cirrhosis. 673 66

Diffuse nodular regenerative hyperplasia of the liver (NRH) is a rare cause of portal hypertension. It is characterized by diffuse nodularity of the liver without cirrhosis. NRH is usually associated with other diseases, most commonly Felty's syndrome. A case is reported in which maturity-onset diabetes mellitus was accompanied by elevated serum insulin levels. Hepatotrophic hormones such as insulin or glucagon may play a role in the development of some cases of NRH.
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PMID:Nodular regenerative hyperplasia of the liver in a patient with diabetes mellitus. 705 13

Glucagon has been proposed as the mediator of splanchnic hyperemia in portal hypertension. Employing an assay specific for pancreatic glucagon, we reevaluated the relationship between this peptide and portal hypertension in the portal vein (PV)-stenosed rat model addressing, in particular, the effects of anesthesia and surgical stress. Plasma glucagon levels were similar in sham-operated and portal hypertensive rats: glucagon, sham vs PV stenosed: 110.7 +/- 17.1 pmol/liter vs 140.6 +/- 23.3 pmol/liter (NS). Furthermore, plasma levels of glucagon and the related peptide VIP were not significantly influenced by anesthesia or surgical stress, and levels remained similar under all conditions in sham-operated and PV-stenosed animals. We conclude that pancreatic glucagon is not elevated in the PV-stenosed rat; differences between these results and those describing hyperglucagonemia in this model cannot be explained on the basis of a differential response to stress but may reflect differences in glucagon assay system.
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PMID:Glucagon, stress, and portal hypertension. Plasma glucagon levels and portal hypertension in relation to anesthesia and surgical stress. 764 85

Among the general principles of the therapy of hepatic encephalopathy the authors discuss the intensive care of patients, maintenance of their volume and electrolyte balance, treatment of coagulation defect, therapy of gastrointestinal bleeding and portal hypertension, provision of central renal catheter, infection prophylaxis, monitoring of intracranial pressure, and if necessary, respiration and intubation of patients. The study also deals with possibilities of treatment based on the toxic hypothesis and on the theory of neurotransmitters. Attention is paid to the therapy of brain oedema and to the significance of hemodialysis, hemoperfusion, plasmapheresis and hybrid bioartificial liver cell treatment. The authors deal with the indications of glucagon-insulin therapy and emphasize the importance of liver transplantation in the treatment of hepatic encephalopathy.
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PMID:[Management of hepatic encephalopathy]. 774 57

Liver cirrhosis is characterized by an increased incidence of glucose intolerance, diabetes and insulin resistance. We report a cirrhotic man (41 years old) who developed glucose intolerance and diabetes with insulin resistance over a period of six years. This patient suffered from severe portal hypertension with oesophageal varices and a enormously increased spleen volume. The subject underwent prophylactic endoscopic sclerotherapy of oesophageal varices. Splenectomy was performed because of severe piastrinopenia with recurrent nose bleeding. During laparotomy, multiple liver biopsies confirmed diagnosis of liver cirrhosis. Intra-operatory exploration revealed a splenic vein thrombosis. For this reason the planned spleno-renal shunting was not performed and the patient was only submitted to splenectomy. Liver function improved in the month following splenectomy and concomitant decrease of insulin resistance was observed (with a reduction in daily insulin dosage from 126 to 10 I.U.). We propose the following explanations of this event: 1) A decrease of portal and pancreatic vein pressure may have induced a proportional decrease (as already reported) of glucagon secretion. 2) The ameliorated liver function may have induced an improvement of liver glucose, insulin and glucagon metabolism. 3) A reduction of insulin circulating level (proved by a decrease of C Peptide value) may have lessened the insulin receptor down-regulation.
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PMID:[Decrease of insulin resistance after splenectomy in a diabetic patient with liver cirrhosis and portal hypertension. Physiopathologic evaluation]. 784 51

This study was designed to investigate the effect of octreotide (Sandostatin, Sandoz), an analogue of somatostatin, on the hemodynamics and glucagon level in portal hypertension. Sixteen portal hypertensive rabbits produced by partial ligation of the portal vein two weeks earlier received an intravenous infusion of octreotide at a dose of 30 micrograms/h. After infusion of octreotide, a significant reduction in portal venous pressure from 16.2 +/- 3.9 mmHg (mean +/- SD) to 13.3 +/- 4.3 mmHg at 21 minutes and 12.0 +/- 4.5 mmHg 42 minutes was noted. A persistent decrease in portal pressure to 11.0 +/- 4.5 mmHg 21 minutes after stopping infusion of octreotide was also observed. Portal venous blood flow was decreased significantly from 60.9 +/- 13.1 mL/min to 46.9 +/- 15.0 ml/min at 21 minutes and to 45.8 +/- 12.8 ml/min at 42 minutes. A slight elevation of portal blood flow to 49.0 +/- 14.1 ml/min was noted 21 minutes after cessation of octreotide infusion. Portal venous resistance was slightly elevated during infusion of octreotide (before infusion: 2.2 +/- 1.4 dyne.s.cm-5, 21 minutes after infusion: 2.4 +/- 1.4 dyne.s.cm-5 and 42 minutes after infusion: 2.3 +/- 1.3 dyne.s.cm-5), and decreased (1.9 +/- 1.0 dyne.s.cm-5, p < 0.1) with a forward significance after stopping infusion. There were no significant changes in systemic arterial pressure during this experiment. A significant decrease (p < 0.05) in glucagon level from 323 +/- 93 pg/dl to 267 +/- 62 pg/dl at 21 minutes and to 298 +/- 88 pg/dl at 42 minutes in the portal vein was noted during the infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of octreotide on hemodynamics and glucagon levels in portal hypertensive rabbits. 785 49


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