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)

In view of the importance of insulin in hepatic cell proliferation and regeneration, disturbances might be expected in these processes in diabetics. The relative importnace of insulin replacement given intraportally rather than subcutaneously is discussed. Results are presented showing that even when normoglycaemia is achieved with peripheral insulin infusion using the 'artificial pancreas' there are still abnormalities in intermediary metabolism. The incidence of cirrhosis in diabetes is reviewed and it is concluded that the evidence is poor for an increase in diabetics. Finally it is shown that in the normal diabetic rat changes are observed after partial hepatectomy consistent with an increase in redox potential within the regenerating liver. Insulin treatment improves redox status but does not completely reverse the changes shown.
 ...
PMID:Hepatotrophic factors: implications for diabetes mellitus. 24 6

Insulin degradation was measured by the C-peptide/insulin ratio in 19 patients with portal vein block with extensive spontaneous portal-systemic shunting but minimal liver cell damage: 13 patients with biopsy-proved cirrhosis and 12 controls. Blood obtained fasting and for 3 hr after oral glucose was assayed for glucose, insulin, and C-peptide. Fasting C-peptide and insulin levels in patients with portal vein block and those in controls did not differ. Eight of 13 cirrhotic patients had fasting hyperinsulinemia with a significantly reduced C-peptide/insulin ratio. After glucose administration, the C-peptide/insulin ratio in portal vein block patients with normal aspartate transaminase levels did not differ from control values. In portal vein block patients with elevated asparatate transaminase levels, the C-peptide/insulin ratio was significantly reduced only from 60 min onwards. All the cirrhotic patients showed a significantly reduced C-peptide/insulin ratio after glucose administration. It is suggested that portal-systemic shunting of blood in the presence of a normal liver does not influence hepatic insulin metabolism and that the hyperinsulinemia of cirrhosis is a feature of parenchymal liver damage. In addition, insulin degradation was abnormal in all cirrhotic patients at high insulin secretion rates, even when fasting insulin levels were normal.
 ...
PMID:Effects of spontaneous portal-systemic shunting on insulin metabolism. 42 95

Blood sugar, insulin and GH values were examined in two groups of cirrhosis of the liver patients, with and without ascites, after the administration of 100 g glucose per os. No significant differences between the two groups were observed. Insulin values were higher than those in the controls, with a pattern similar to that noted in subjects with chemical diabetes. GH values were higher than in normal subjects and secretion was not suppressed.
 ...
PMID:[Plasma insulin and GH during oral glucose load in liver cirrhosis]. 95 Oct 48

Decreased increases in blood sugar by comparison with control subjects was noted in patients with cirrhosis of the liver after i.v. administration of 1 mg glucagon. Insulin secretion was similar to that observed in the controls. Basal GH values were higher in the liver patients, whereas after glucagon they displayed a gradual and progressive increase with a peak at 60'. No significant differences in GH pattern were noted in the two groups, however.
 ...
PMID:[Changes in plasma insulin and growth hormone after intravenous glucagon in hepatic cirrhosis]. 99 78

An intact pituitary gland capable of secreting growth hormone has long been considered the prime requirement for the achievement of skeletal growth potential in man. Recent studies have revealed that the growth-promoting action of growth hormone is an in-vivo phenomenon which cannot be mimicked by the addition of the hormone to skeletal tissue in vitro. The humoral agent responsible for skeletal growth has now been identified as somatomedin, a peptide produced in the liver under the stimulus of pituitary growth hormone. Serum levels of somatomedin are measured in a bioassay system by monitoring the stimulation of uptake of labelled sulphate by cartilage. Low levels of somatomedin activity are detected in the serum of children with growth hormone deficiency and short stature; the levels are high in acromegalics and low in patients with cirrhosis of the liver or chronic renal failure. Undernourished children also have low levels despite reaised serum levels of growth hormone; this suggests the presence of an inhibitor which lowers the growth-promoting activity of the somatomedin molecule. Adequate nutrition in these children results in the restoration of serum somatomedin levels to normal. Attempts to isolate and purify somatomedin have led to the identification of a group of substances sharing similar actions on skeletal tissue. Insulin has also been demonstrated to share some of these growth-promoting activities but varies in its organ specificity. Nerve growth factor, epidermal growth factor and proinsulin are other molecules which form a large group of growth promoting peptides which may all be related to the somatomedins.
 ...
PMID:Somatomedins. 115 75

Insulin concentration in the peripheral blood and the thoracic duct lymph from male rabbits with CCl4-induced liver cirrhosis was measured using a radioimmunoassay technique. Although insulin concentration in the lymph was lower in the cirrhotic animals than in the control ones, the hourly transport of the hormone by the lymphatic vessel of the cirrhotic animals markedly increased in company with the higher flow rate of the lymph.
 ...
PMID:Insulin transport by thoracic duct of male rabbits with CCI4-induced liver cirrhosis. 123 97

Insulin binding and insulin receptor down-regulation characteristics were evaluated, as well as cholesterol and phospholipid levels in erythrocytes from 22 patients with liver cirrhosis. These parameters were correlated with clinical characteristics and with scores related to severity of the liver injury. Nine healthy subjects were studied as a control group. It was observed that insulin binding was generally greater in patients than in controls because of an increase in surface insulin receptor numbers, rather than from a change in receptor affinities. In cirrhotic patients, the erythrocyte insulin receptors did not undergo the normal down-regulation process but, in most cases, increased in response to insulin incubation. The alterations in insulin processing characteristics were more frequent in patients with alcoholic cirrhosis and more severe liver impairment and correlated with the changes in the lipid composition of erythrocyte membranes. In particular, an increase in the cholesterol to phospholipid molar ratio and a decrease in polyunsaturated fatty acid content of phospholipids in erythrocyte membranes of cirrhotic patients was associated with impairments in insulin receptor processing. Similar changes in insulin receptor processing were observed when the molar ratio of cholesterol to phospholipid in normal erythrocytes was modified in vitro by incubation with cholesterol-rich liposomes.
 ...
PMID:Altered insulin receptor processing and membrane lipid composition in erythrocytes of cirrhotic patients. 157 65

Insulin-induced glucose metabolism was investigated in 26 patients with biopsy-proven liver cirrhosis and 10 control subjects. Two glucose clamp protocols together with continuous indirect calorimetry were performed to examine whether reduced rates of glucose oxidation and/or nonoxidative glucose metabolism explain insulin resistance in liver cirrhosis. Using a 4-hour, two-step protocol (0-2 hours, plasma glucose 5.2 mmol/L, plasma insulin 92 mU/L to test the half-maximum response; 2-4 hours, hyperglycemia 10.0 mmol/L, plasma insulin 442 mU/L to test the maximum cellular glucose disposal) liver cirrhosis reduced glucose disposal to 45% and 60% of control values, respectively. Simultaneously, insulin-induced increases in glucose oxidation, plasma lactate levels, and lipogenesis were normal, whereas nonoxidative glucose metabolism was reduced (-82% and -47% of controls, respectively). To determine whether reduced nonoxidative glucose metabolism was caused by reduced glucose disposal, glucose disposal was "matched" to normal values in a subgroup of cirrhotic patients. Nonoxidative glucose metabolism values were normal, but plasma lactate concentrations disproportionally increased (+96%) after "matching" glucose disposal. Insulin resistance was independent of the etiology of the cirrhosis, the biochemical parameters of parenchymal cell damage and liver function, and the clinical and nutritional state of the patients. It is concluded that liver cirrhosis impairs insulin sensitivity and maximum cellular glucose disposal. Reduced glucose disposal is caused by defective glucose storage. Insulin resistance is independent of the etiology of liver cirrhosis and of the clinical and nutritional state of the patient.
 ...
PMID:Mechanism of insulin resistance associated with liver cirrhosis. 158 21

A 58-year-old man, with primary hemochromatosis, cirrhosis, and diabetes mellitus treated with insulin developed hepatoma. As the tumor grew, he lost his dependence on insulin therapy and experienced episodes of hypoglycemia. His response to infuse insulin was studied using the euglycemic clamp technique. Insulin was infused at rates of 1 and 10 mu/kg/min. The insulin dose response curve was shifted to the left and at plasma insulin levels of 72 microU/ml, steady-state glucose consumption was 9.6 mg/kg/min, 50% more than in normals, and nearly three times greater than that in other cirrhotics. The insulin clearance rate was 4417 m1/m2/min, almost five and six times more than in normals and cirrhotics, respectively. Basal hepatic glucose production was 3.6 mg/kg/min, two and three times higher than in normal and in cirrhotic subjects, respectively. The decrease in amino acid during hyperinsulinemia was more than 30% higher than in normal and other cirrhotics. IFG-I and II levels were not elevated in this patient. Increased insulin sensitivity and increased insulin clearance and serum amino acid decrease in response to insulin in vivo, suggest that insulin responsive tissues are at last partially responsible for tumor hypoglycemia. The increased glucose disposal rate probably accounted for the disappearance of the diabetes.
 ...
PMID:Case report: increased insulin sensitivity in tumor hypoglycemia in a diabetic patient: glucose metabolism in tumor hypoglycemia. 165 53

Insulin action was studied in rats with CCl4/phenobarbital-induced cirrhosis of the liver using the euglycemic hyperinsulinemic clamp technique coupled with isotopic measurement of individual tissue glucose uptake, glycogen formation, and lipogenesis. In cirrhotic rats, dose response curves showed a reduction of insulin-stimulated total body glucose disposal of about 30%. Insulin action on tissue glucose uptake and initial phosphorylation (assessed with [3H]2-deoxyglucose) were unchanged; however, incorporation of [14C]glucose into lipids and particularly into glycogen was reduced substantially (being most pronounced in skeletal muscle and diaphragm) at maximally as well as half-maximally effective serum insulin concentrations during euglycemic clamping. At identical IV insulin infusion rates, steady-state serum insulin concentrations were elevated up to fourfold in cirrhotic animals. Antilipolytic action of insulin was unaltered. These data suggest that the principal metabolic pathway affected in insulin resistance of rats with experimental cirrhosis appeared to be insulin-stimulated glycogen formation in muscle tissues.
 ...
PMID:Mechanism of insulin resistance in CCl4-induced cirrhosis of rats. 172 57


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