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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute pancreatitis often results in a hyperdynamic, consumptive state. Hallmarks of this condition are decreased peripheral resistance with increased cardiac output. Hemodynamic and cardiovascular changes are accompanied by metabolic alterations. Increased protein catabolism, increased ureagenesis, glucose intolerance, increased lipolysis, and reduced servoregulation are metabolic changes commonly seen in this syndrome. To preserve organ structure and function, biochemical processes must be metabolically supported. Substrate needs change as stress level increases. The per cent of total calories provided as protein must increase. Branched-chain-enriched amino acid solutions have been shown to improve nitrogen utilization in hypermetabolic patients and may therefore be beneficial for the patient with acute pancreatitis. Glucose utilization decreases and free fatty oxidation increases. A mixed fuel system that provides fat, protein, and glucose is suggested for these patients. IV fat has been shown to be a safe energy substrate for patients with pancreatitis in the absence of hyperlipidemia. Failure to use fat as an energy substrate in conjunction with TPN may result in hepatic steatosis and excess carbon dioxide production. The decision of whether to use the parenteral or enteral route to nutritionally support the patient with pancreatitis remains controversial. TPN may allow maintenance of pancreatic rest. The role of enteral feedings is less clear. However, it has been shown that the further down the alimentary tract the feeding is infused, the less pancreatic stimulation occurs. Therefore, it seems wise to support the patient with TPN during severe acute pancreatitis. Jejunal enteral feedings should be initiated as a transitional feeding when the acute inflammatory episode begins to subside.
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PMID:Nutritional support in acute pancreatitis. 250 54

Evidence of hepatic dysfunction (clinically, chemically, and morphologically) and biliary-tract abnormalities is common in patients receiving TPN. The entity might present as hepatocellular injury (fatty liver, steatonecrosis), intrahepatic cholestasis, acalculous cholecystitis, or cholelithiasis. Infants manifest primarily intrahepatic cholestasis, whereas adults manifest fatty liver early and intrahepatic cholestasis later in the course of therapy. Both groups are at risk for the development of biliary-tract abnormalities. Although most of these changes in the adult are mild and reversible, a small number of patients have recently been reported to develop progressive liver disease. In infants, however, the changes may be more severe, and lead more frequently to progressive liver disease and death. Although this progression to chronic liver disease is worrisome, it is uncertain whether, in patients on long-term therapy, it is due to the TPN or to other conditions or therapies associated with their clinical condition. The pathogenesis of each of these lesions may be multifactorial, including carbohydrate overfeeding, essential-fatty-acid deficiency, amino-acid deficiencies or imbalances, carnitine deficiency, bile-salt toxicity, lipid emulsions, bile-flow reduction, and gallbladder stasis. Therapies in these patients are aimed at alterations in the preceding etiologies (decreased glucose loads, contraction of the gallbladder). Further work is necessary to delineate the exact mechanisms of this entity, especially with regard to the causal relationships of TPN and this entity and to the development of chronic liver disease.
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PMID:Hepatobiliary abnormalities associated with total parenteral nutrition. 250 58

In a large sample of 1379 adult patients and, in addition, in a smaller group of 223 other patients in whom a glucose tolerance test with measurement of serum insulin was carried out, an increase of blood pressure, pulse rate, relative body weight and serum insulin was found which correlated significantly with that range of gamma glutamyltransferase (GGT) values which erroneously so far is considered to be normal. The really normal range of the GGT is not up to 28 (measured at 25 degrees C), but only up to 10 U/l. Persons with GGT 9-12 U/l have a significantly higher blood pressure than persons with GGT up to 8 U/l. The relationship between blood pressure and GGT is the same in males and females although the females show a higher GGT for the same amount of alcohol consumed; in both, males and females, the steepest increase is just in the low GGT range between 9 and 25 U/l. The nature of this ethanol-effect is toxic, not caloric. Daily alcohol in "normal" ("social") amounts causes hyperinsulinemia (and thus increased sodium reabsorption in the Kidney) as well as increased catecholamine excretion. "Normal" alcohol consumption leading to hepatic steatosis as the "normal" condition of the population, has more health hazards than so for assumed. A GGT higher than 10 U/l (measured at 25 degrees C), is besides hyperinsulinemia the most sensitive test for pathologic changes of the metabolism and the cardiovascular parameters due to hepatic steatosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The normal values of gamma-glutamyltransferase are falsely defined up to now: on the diagnosis of hypertension, obesity and diabetes with reference to "normal" consumption of alcohol]. 256 44

1. Male Mongolian gerbils (Meriones unguiculatus) liver activates CCl4 to free radicals that bind covalently to cellular components (CB) and stimulate a lipid peroxidation (LP) process to a larger extent than the rat liver. 2. CCl4 administration results in a less intense necrogenic effect in gerbils than in rats and does not cause fatty liver. 3. CCl4 causes less intense effects on liver ultrastructure or calcium metabolism but more marked depression of glucose 6 phosphatase activity (G6P-ase) in gerbils than in rats. 4. Results suggest that a better ability of gerbil liver to keep calcium homeostasis than rat liver might be the cause of their relative resistance to necrosis. Higher intensity of CB and LP in gerbils than in rats might explain more intense effects on G6P-ase.
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PMID:Carbon tetrachloride-induced liver cell injury in the Mongolian gerbil (Meriones unguiculatus). 257 75

Feed restriction and dietary 1,3-butanediol were used with lactating goats in an attempt to induce metabolic changes characteristic of bovine lactation ketosis and fatty liver. In Experiment 1, midlactation goats were fed 80, 102, or 114% of metabolizable energy requirements and 0, 50, or 100 g/d of 1,3-butanediol. Concentration of beta-hydroxybutyrate in blood plasma decreased with increasing metabolizable energy but was increased greatly at 2 h after goats were fed 50 or 100 g butanediol and remained elevated at 6 h postfeeding with 100 g of butanediol. Concentration of glucose in plasma was decreased at 2 and 6 h postfeeding in goats fed 100 g of butanediol. In Experiment 2, goats in early lactation were fed for ad libitum intake or were restricted to 70% of ad libitum intake with 1,3-butanediol included at 10% of diet DM. The treatment decreased milk production, increased concentrations of beta-hydroxybutyrate and nonesterified fatty acids, and decreased the concentration of insulin and the insulin to glucagon ratio in plasma. Concentrations of glucose, acetate, and glucagon in plasma were not affected. After 28 d of treatment, concentration of total lipid in liver was increased, but concentrations of glycogen and triglyceride were unaffected. Changes caused in goats by feed restriction plus dietary 1,3-butanediol were characteristic of subclinical lactation ketosis in cows, but the response was more moderate than seen previously in cows.
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PMID:Metabolic responses of lactating goats to feed restriction and dietary 1,3-butanediol. 262 43

We report the case of a 25-year-old nullipara in whom polyuria and polydipsia occurred 8 weeks before the first symptoms of acute fatty liver of pregnancy and disappeared a few days after delivery. This time course suggests that polyuria and polydipsia were closely related to acute fatty liver of pregnancy. Thus, this diagnosis should be envisaged in any woman with normal blood levels of glucose and calcium, and complaining of polyuria and polydipsia in the third trimester of pregnancy.
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PMID:[Polyuria and polydipsia in acute fatty liver of pregnancy. Discussion based on a case]. 271 1

To elucidate if the presence of fatty liver and hypertriglyceridemia (HTG) influences pancreatic A-cell function in obesity, basal and arginine-stimulated glucagon (IRG) secretions were studied in 7 normal subjects and in 28 moderately obese patients (OB) with normal glucose tolerance. The patients were divided into 4 groups, based on the presence of fatty liver and/or HTG. BMI was similar in all four obese groups. Basal IRG, as well as the sum of secretory response to arginine, namely sigma IRG values, were significantly (p less than 0.01) higher in the OB subgroup having both fatty liver and HTG than in the other three groups; these values were similar in subgroups of OB without fatty liver, and showed no significant difference from the normals. Basal and sigma IRG values in all OB correlated well with the degree of fatty liver and HTG, demonstrating that by stepwise analysis the effects of fatty liver and HTG were independent for basal and sigma IRG values. These results suggest that the combination of fatty liver and HTG may serve as a good predictor of hyperglucagonemia in simple obesity, and, hence, metabolic heterogeneity among obese patients should be considered in evaluating A-cell function.
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PMID:Elevated pancreatic glucagon in moderately obese patients: relationship of fatty liver and hypertriglyceridemia. 273 44

In a cross-sectional health screening 636 persons with negative urine glucose, a 75-g-oral glucose tolerance test was performed. We report the clinical features of the subjects with impaired glucose tolerance or diabetes mellitus. In 96 subjects with impaired glucose tolerance, the frequencies of alcohol dependency, fatty liver, and of increased levels of serum uric acid, cholesterol, triglycerides, total serum protein and gamma-glutamyl transpeptidase were significantly higher than in normal subjects. In 37 subjects with diabetes mellitus, the frequencies of fatty liver, hypertension and of increased erythrocyte sedimentation rate, triglycerides and gamma-glutamyl transpeptidase were significantly higher than in normal subjects. In addition, significant increases in serum gamma-glutamyl transpeptidase, triglycerides, serum total cholesterol and body mass index, and a significant decrease in high density lipoprotein cholesterol were also observed in subjects with impaired glucose tolerance and diabetes mellitus. These results suggest that alcohol dependency, fatty liver, obesity and hyperlipidemia are important concomitants of impaired glucose tolerance.
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PMID:Study on background factors associated with impaired glucose tolerance and/or diabetes mellitus. 278 10

Injection of hydrazine (0.7 mmole/kg) in the male fasting rats caused an increase in phosphatidate phosphohydrolase (PAP) activity in the soluble fraction of the liver. The increased PAP activity was parallel with a rise in hepatic triacylglycerol (TG) (3.5-fold) and in the catecholamine concentration (3.4-fold) in adrenal glands. Hydrazine also increased serum glucose. The hydrazine-induced increase in PAP activity and TG accumulation was completely prevented by adrenalectomy. The data suggest that increased PAP activity is at least partly responsible for hydrazine-induced fatty liver and that adrenal hormones may take part in the mechanism by which hydrazine exerts its effects on the liver.
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PMID:The effects of hydrazine on the phosphatidate phosphohydrolase activity in rat liver. 303 6

To elucidate if the presence of fatty liver in obesity influences hepatic insulin extraction under basal conditions, serum immunoreactive insulin (IRI) and C-peptide immunoreactivity (CPR) were measured in 20 obese patients with normal glucose tolerance and in 8 normal subjects. The obese patients were subdivided into two groups matched for age and body weight according to the presence or absence of fatty liver: 8 obese patients without fatty liver (OBN) and 14 with fatty liver (OBF). Basal levels of IRI and CPR were significantly greater in the obese patients than in the normals, but were similar in the two obese groups. In the OBF group, the CPR/IRI molar ratios, a relative measure of hepatic insulin uptake, were significantly lower than in the other two groups, while the ratios of the normal and OBN groups were similar. The CPR/IRI molar ratios in all obese patients correlated well with the degree of fatty liver (r = 0.785, p less than 0.001). These results suggest that hepatic insulin extraction in a subgroup of obese patients is either reduced or indistinguishable from that of non-obese subjects, and that basal CPR/IRI molar ratio may serve as a useful indicator of the presence of fatty liver in simple obesity.
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PMID:Altered basal C-peptide/insulin molar ratios in obese patients with fatty liver. 305 68


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