Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma insulin, glucagon, somatostatin, and glucose concentrations were measured in the fasting state as well as after mixed meals (breakfast, lunch, and dinner) in 10 cirrhotic patients and 10 control subjects during a 24-hour period. Cirrhotic patients had fasting glucose values higher than controls (at -15 min: 5.2 +/- 0.2 mmol/L v 3.9 +/- 0.5 mmol/L, P less than 0.05; at 0 min: 5.5 +/- 0.3 mmol/L v 4.3 +/- 0.5 mmol/L, P less than 0.01). After meals blood glucose values remained higher in cirrhotics than in controls. Insulin levels did not differ between the groups in the fasting state, but cirrhotics showed a lower response to meals. Corresponding glucagon concentrations were greater in cirrhotics than in controls before and after meals throughout the 24-hour period (from -15 min to 24 hour: P less than 0.01). BAsal plasma somatostatin levels in the cirrhotic group were significantly higher than in control subjects (at -15 min and at 0 min: P less than 0.05) and further increased after meals. Plasma somatostatin was heterogeneous in normal and cirrhotic group, but the increase in its concentrations in patients with chronic liver disease was for the most part a consequence of elevations in the 1600 and 3500 molecular weight components. The half-life of exogenously infused somatostatin in cirrhotics was comparable to that of controls. These results indicate that in liver cirrhosis elevated levels of circulating somatostatin are associated with hyperglucagonemia and impaired insulin release. The high plasma somatostatin levels observed in cirrhotic patients are the result of hypersecretion of the D cell rather than impaired removal of the peptide.
 ...
PMID:Circulating somatostatin concentrations in healthy and cirrhotic subjects. 286 81

The influence of a long-acting somatostatin octapeptide analogue (SMS 201-995) on splanchnic circulation and metabolism has been studied in healthy subjects and in patients with liver cirrhosis. In healthy subjects doses of 5, 10, 50, or 100 micrograms SMS and in the cirrhotic patients 25 micrograms SMS were infused intravenously during 1 h. Measurements were obtained before, during, and for 1 h after SMS infusion. SMS infusion in healthy subjects resulted in a 25-35% reduction in hepatic blood flow. This effect was largely independent of the dose used. Splanchnic oxygen uptake was unchanged before and during SMS infusion. Insulin and glucagon levels fell markedly in response to SMS administration, and the blood concentration and splanchnic output of glucose decreased transiently. Patients with liver cirrhosis responded to SMS infusion similarly to the healthy subjects. Hepatic blood flow decreased by 25-35% and remained suppressed for at least 1 h after infusion. Wedge hepatic venous pressure was 18 +/- 2 mm Hg in the basal state and decreased progressively during and after SMS infusion (60 min after infusion, 15 +/- 2 mm Hg; P less than 0.01). The marked hyperinsulinaemia and hyperglucagonaemia seen in the basal state decreased significantly during SMS administration. As in the case of the controls, blood concentration and splanchnic output of glucose fell transiently during and after SMS infusion. It is concluded that SMS exerts a marked and prolonged suppressive effect on hepatic blood flow in both healthy subjects and patients with liver cirrhosis.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The influence of a long-acting somatostatin analogue on splanchnic haemodynamics and metabolism in healthy subjects and patients with liver cirrhosis. 287 92

The aim of this study was to evaluate the contribution of gluconeogenesis from amino acids in the development of fasting and absorptive hyperammonemia in cirrhosis. Somatostatin (SRIF), which is known to inhibit the hepatic disposal of gluconeogenic amino acids, was administered in a continuous infusion (500 micrograms/h) for 90 min before and 5 h after a protein meal (240 g of meat) in 11 overnight fasting patients. Plasma glucagon, insulin, gluconeogenic amino acids (GAA: alanine, serine, glycine, and threonine) and ammonia (NH3) were evaluated before the infusion, immediately before, and at 1, 3, and 5 h after the meal. As control study, the same protocol was randomly repeated in a different day with saline infusion. During the latter, a direct correlation was found between fasting glucagon and ammonia (r = 0.68; p less than 0.05). Fasting glucagon, insulin, and NH3 did not change, whereas alanine (p less than 0.05) and the GAA sum decreased (p less than 0.01). When SRIF was infused, fasting glucagon (p less than 0.05), insulin (p less than 0.05), and NH3 (p less than 0.05) decreased. Alanine did not change, and GAA sum increased (p less than 0.02). No correlations were found by plotting changes in glucagon or GAA sum and NH3. After the meal, SRIF infusion abolished the plasma response of glucagon and markedly reduced that of insulin, so that their area under the curve (AUC0-5) were reduced (p less than 0.005, for both), with respect to control study. Moreover, the AUC0-5 of alanine (p less than 0.005) and GAA sum (p less than 0.005) were increased, suggesting a reduced disposal of these compounds. In spite of this, the meal-induced early increase and the AUC0-5 of plasma NH3 observed during SRIF and saline infusion did not differ. Our results do not confirm the importance of gluconeogenesis from alpha-amino-nitrogens in determining the fasting ammonemia of cirrhosis, and suggest that this metabolic pathway does not significantly influence the protein meal-induced exacerbation of plasma ammonia.
 ...
PMID:Role of gluconeogenesis from amino acids in determining fasting and absorptive levels of plasma ammonia in cirrhosis. 289 85

The present study was undertaken in order to establish the significance of glucagon in glucose intolerance in liver cirrhosis. The plasma glucose response to an oral glucose load (75 g) was determined in 10 control subjects and in 10 cirrhotic patients, after infusions of: glucagon (3 ng.kg-1.min-1) or saline (154 mmol/l); somatostatin (SRIH) (500 micrograms/h); and SRIH plus glucagon (3 ng.kg-1.min-1). Glucagon infusion did not impair glucose tolerance, neither in normal subjects nor in patients with cirrhosis. On the other hand, in both groups glucose tolerance was impaired by SRIH infusion, presumably owing to an absolute insulin deficiency. Both in normal subjects and in cirrhotic patients, SRIH plus glucagon infusion further impaired glucose tolerance, presumably as a result of excess glucagon and concomitant insulin deficiency. In conclusion, our data show that hyperglucagonemia is not an important factor in the development of the glucose intolerance in patients with hepatic cirrhosis.
 ...
PMID:Glucagon and glucose tolerance in liver cirrhosis. 289 68

The effect of glucagon on hepatic regional hemodynamics was investigated in patients with chronic liver disease during peritoneoscopy with reflectance spectrophotometry. When glucagon was infused intravenously in patients with a non-cirrhotic liver, the regional hepatic tissue oxygen consumption, as estimated spectrophotometrically, increased significantly, whereas the index of hepatic tissue blood volume did not change appreciably, and consequently, the oxygen saturation of hemoglobin in the hepatic tissue blood decreased. In contrast, the administration of glucagon in patients with liver cirrhosis resulted in a significant increase in the index of hepatic tissue blood volume and produced a minor increase in hepatic tissue oxygen consumption. The oxygen saturation of hepatic blood hemoglobin tended to increase in the cirrhotics. The result suggests the presence of functional vasoconstriction at the presinusoidal and/or sinusoidal vessels in the cirrhotic liver, possibly due to a decreased vasomotor activity and/or an abnormal regulatory function of vasoactive substances, which are released by glucagon.
 ...
PMID:Characterization of hepatic hemodynamics in cirrhotics and non-cirrhotics. Effect of glucagon infusion. 292 37

In order to elucidate the response of plasma glucagon in liver cell carcinoma, a clinical study was performed in 12 patients with liver cell carcinoma in addition to 8 patients with liver cirrhosis and 8 normal subjects. Arginine infusion elicited increases in plasma insulin and glucagon in 6 patients with liver cell carcinoma as well as 8 patients with liver cirrhosis compared with the controls. However, the responses of plasma insulin and glucagon in liver cell carcinoma did not exceed those in liver cirrhosis. No glucagon secreting cell was proved in the hepatic cancer tissues from two other patients. Furthermore, no measurable glucagon was demonstrated in the tumor tissues extracted from four other patients with liver cell carcinoma. The extract of the tumors, infused into the pancreatic artery of anesthetized dogs, did not elicit any discernible changes in glucagon and insulin in the pancreatic vein. The present study demonstrates an elevated response of plasma glucagon in liver cell carcinoma. Since the morphological and biochemical studies failed to demonstrate the glucagon secreting cell or glucagon-stimulating material in the tumor tissues, the elevated plasma glucagon response might be interpreted by the increased A-cell function of the pancreas and the decreased degradation of the hormones in the liver.
 ...
PMID:Secretion of glucagon in liver cell carcinoma. 299 19

Levels of plasma cyclic AMP, serum immunoreactive insulin (IRI), serum c-peptide immunoreactivity (CPR) and blood sugar (BS) were determined 0, 15, 30, 45 and 60 min after a glucagon injection (0.01 mg per kg body weight) in normal controls, patients with acute hepatitis and liver cirrhosis. Plasma cyclic AMP responses to glucagon in liver disease patients varied widely in peak value, and only in patients with fulminant hepatitis and decompensated liver cirrhosis with poor prognosis was the response suppressed. The peak response of BS was found significantly later in liver cirrhosis patients than in normal controls. IRI and CPR responses to glucagon were lower in acute hepatitis patients than in normal controls and liver cirrhosis patients. IRI levels and their sum were also lower in acute hepatitis patients, although CPR levels were not significantly different. Thus, the ratio of the sum of CPR from 0 to 60 min to that of IRI was significantly higher in acute hepatitis, indicating impaired pancreatic secretion of insulin to glucagon stimulation as well as increased uptake of insulin by the liver in acute hepatitis.
 ...
PMID:Responses of plasma cyclic AMP, serum immunoreactive insulin, C-peptide immunoreactivity and blood sugar levels to glucagon in patients with liver diseases. 300 Jan 42

Pancreatic endocrine function in liver cirrhosis was examined in rats both in vivo and in vitro. Experimental liver cirrhosis was induced by subcutaneous injections of 50% carbon tetrachloride in a dose of 2 mL/kg body weight twice a week for 16 weeks. Control rats received a similar dose of olive oil during the same period. In cirrhotic rats, immunoreactive insulin contents in the pancreas were significantly lower, whereas immunoreactive glucagon contents were about threefold higher than those of control rats. In the first part of this study, insulin and glucagon concentrations in both jugular and portal venous blood at basal conditions and after oral glucose loading were simultaneously determined in vivo. Peripheral insulin levels, both before and after glucose loading, were higher, whereas portal insulin concentrations were lower in cirrhotic rats than in the control rats. In contrast, glucagon levels in both the peripheral and portal veins were significantly higher in cirrhotic rats than in control rats. In the second part, isolated perfused pancreata were prepared from cirrhotic and control rats to further characterize the endocrine function of cirrhotic rat pancreas. Insulin secretion in response to 16.7 mmol/L glucose and 100 pmol/L cholecystokinin-octapeptide both were 40% lower in cirrhotic rats than in controls. In contrast, there was no significant difference in arginine-stimulated insulin release between the two groups. However, glucagon secretion in response to 20 mmol/L arginine was 40% higher in cirrhotic rats. If sensitivity is defined as the hormone release proportional to the pancreatic contents, then A and B cells in the cirrhotic rats had normal sensitivity to both glucose and cholecystokinin-octapeptide.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Pancreatic endocrine function in cirrhotic rats. 304 24

In addition to direct toxic effects on endocrine organs chronic alcohol intake affects regulation of endocrine systems by disturbed liver function. As a result in patients with alcohol-induced liver cirrhosis gonadal axis is characterized by low total and free testosterone, elevated estradiol. LH, FSH, and sexual hormone binding globulin and an enhanced conversion of testosterone to estradiol. Prolactin also is found to be elevated. The thyrotropic axis is characterised by low T3- und T4- as well as elevated rT3-values and normal TSH. STH is elevated, while somatomedin C is decreased. The corticotropic axis may show an abolished circadian rhythm, a negative Dexamethasone-test, low transcortin and elevated free cortisol levels. The disturbance of the calcitropic axis leads to osteoporosis and osteomalacia, due to intestinal hyperparathyroidism and vitamin D malnutrition. In 50% of chronic alcoholics there are elevated insulin and glucagon values and a pathological glucose tolerance test.
 ...
PMID:[Alcohol and endocrinologic homeostasis]. 306 42

Insulin (IRI) and C-peptide dynamics were studied after iv glucagon in 5 nondiabetic patients with ascites due to cirrhosis of the liver. Plasma and ascitic fluid samples for glucose, IRI and C-peptide determinations were obtained before and 6, 10, 15, 20 and 30 min after glucagon injection. Ascitic fluid volumes, estimated by dilution of ip injected PAH, were 6.2 to 20.5 L. The mean fasting plasma glucose [88 +/- 6.7 mg/dl (SE)] and C-peptide (1.40 +/- 0.42 ng/ml) levels were normal; mean plasma insulin was increased (17.4 +/- 3.0 microU/ml). After glucagon injection, there was a subnormal rise in plasma glucose (PG) compared to 5 mild diabetic patients without liver disease (8.4 +/- 3.5 vs 76 +/- 7.4 mg/dl). The plasma C-peptide rise was less than that of plasma IRI (54% vs 192%). The mean basal ascitic fluid concentration of glucose was 86 +/- 9.4 mg/dl, IRI 13.2 +/- 2.9 microU/ml and C-peptide 3.09 +/- 0.49 ng/ml. Total calculated basal ascitic fluid contents of glucose was 5.2-23.3 g, IRI 47, 120-290,000 microU and C-peptide 15,750-66,420 ng. These were 3-10 times the quantity of these substances circulating in the plasma volume. After glucagon injection, there was no significant increase in ascitic fluid glucose or IRI, but there was a 43% increase in C-peptide concentration at 10 min. In ascitic fluid, the molar concentration of IRI was lower and C-peptide higher than plasma, resulting in a C-peptide: IRI molar ratio of 11.31, markedly higher than the published normal plasma ratio of 4.63.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Insulin and C-peptide in ascitic fluid and plasma and their relative responses to glucagon in patients with cirrhosis. 306 13


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>