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

Insulin responses to oral glucose loads were studied in patients with obstructive jaundice and compared with those of other liver diseases (fatty liver, chronic hepatitis and liver cirrhosis), pancreatic diseases, and definite diabetes mellitus. Compared with their corresponding glucose intolerance, high insulin responses were characteristic in fatty liver, chronic hepatitis and liver cirrhosis, and insulin responses and insulinogenic index decreased in chronic hepatitis and liver cirrhosis as glucose intolerance progressed. In obstructive jaundice with the pancreatic ducts stenotic or obstructed, insulin responses were suppressed in comparison with their corresponding glucose intolerance, and also insulinogenic index were below 0.5 in most of the cases. However, in obstructive jaundice with the pancreatic ducts intact, high insulin responses were observed in almost half of the cases with insulinogenic index above 0.5, and insulin response and insulinogenic index decreased as glucose intolerance progressed. While most cases of fatty liver, chronic hepatitis and liver cirrhosis with insulinogenic index above 0.5 were distributed in non-diabetes zone in sigma BS-sigma IRI plane (Kosaka's), those with insulinogenic index below 0.5 were distributed in intermediate zone. Most cases with obstructive jaundice with pancreatic ducts stenotic or obstructed, had insulinogenic index below 0.5 and were distributed in diabetes zone. However, half of cases with obstructive jaundice with pancreatic ducts intact, had insulinogenic index above 0.5 and their distribution in non-diabetes zone, while the other half had insulinogenic index below 0.5 and their distribution in diabetes zone. Therefore, it may be concluded that insulin responses increase at the early stage of obstructive jaundice mainly under influence of liver dysfunction itself, but that insulin response is suppressed at later stage of obstructive jaundice as pancreatic islets are affected.
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PMID:[Clinical study on glucose intolerance and insulin response in obstructive jaundice]. 388 96

The effects of late pregnancy on metabolic fuels, liver composition, gluconeogenesis, and nitrogen metabolism have been examined in fed and fasted rats. Plasma free fatty acid (FFA) and immunoreactive insulin (IRI) are greater and glucose and ketones are lower in fed 19-day pregnant than they are in agematched virgin rats. A 48 hr fast elicits greater increases in FFA and ketones and more profound reductions in glucose in the pregnant rats and obliterates the differences in IRI. Fetal weight is not modified by such fasting but maternal weight losses exceed that of the nongravid rats. Livers from rats 19 days pregnant contain more and larger hepatocytes. Per mumole hepatic deoxyribonucleic acid (DNA)-phosphorus, water and protein are more abundant, whereas glycogen is unaffected. Livers from fed pregnant rats contain more lipid phosphorus and less neutral lipid fatty acid. After a 48 hr fast, hepatic steatosis supervenes in gravid animals due to accumulated neutral fat. The contents of hepatic acetyl-coenzyme A (CoA) and citric acid are not different in fed pregnant and virgin rats but are greater in the pregnant rats after fasting. Formation of glucose-(14)C and glycogen-(14)C from administered pyruvate-(14)C are the same in fed pregnant and virgin rats, but greater in the pregnant ones after a 24 or 48 hr fast. Pregnancy does not affect creatinine excretion, and urinary urea is not different in fed pregnant, virgin, and postpartum animals. Contrariwise, more nitrogen, potassium, and phosphorus are excreted by the pregnant animals during a 2 day fast. The increment in urinary nitrogen is due largely to urea on the 1st day, whereas heightened ammonia accounts for half the increase on the 2nd and correlates with the enhanced ketonuria. Muscle catabolism, gluconeogenesis, and diversion to fat are activated more rapidly and to a greater degree when food is withheld during late gestation in the rat. These catabolic propensities are restrained in the fed state. The capacity for "accelerated starvation" may confer survival benefit upon an intermittently eating mother in the presence of a continuously feeding fetus.
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PMID:Carbohydrate metabolism in pregnancy. VI. Plasma fuels, insulin, liver composition, gluconeogenesis, and nitrogen metabolism during late gestation in the fed and fasted rat. 535 39

A maternal survivor of idiopathic fatty liver, with the characteristic histological appearance on liver biopsy, is reported. Profound hypoglycaemia was the major complication in this patient and it is suggested that more attention should be given to the blood glucose in this disease. The consideration of future pregnancy in this patient is discussed.
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PMID:Idiopathic acute fatty liver of pregnancy. 548 32

The effects on lipid metabolism of long-term feeding of large amounts of ethanol or glucose differed from those that have been reported in short-term experiments. Three groups of male rats were investigated. The first was fed lab chow and 15% (v/v) ethanol ad lib.; the second was pair-fed with the first and given isocaloric amounts of glucose in lieu of ethanol; the third was fed lab chow and water ad lib. All three groups consumed nearly the same number of calories, and about 30% of the calories in the first group were derived from ethanol. Neither glucose nor ethanol added to a nutritionally adequate diet promoted the development of a fatty liver, although both stimulated acetate-(14)C utilization for hepatic lipid synthesis. In all three groups more than 80% of the label in hepatic lipid was found in fatty acids, and the distribution of label amongst the fatty acids of different chain lengths was virtually the same. Ethanol decreased while glucose increased the quantity of lipid in fat depots, and each altered the fatty acid composition of the lipids in adipose tissue, kidney, liver, and hepatic subcellular fractions in a different manner. The most striking of these changes was the relative increase in monounsaturated fatty acids and the decrease in essential fatty acids produced by glucose.
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PMID:Effects of prolonged ingestion of glucose or ethanol on tissue lipid composition and lipid biosynthesis in rat. 594 32

1. The influence of ethanol on the metabolism of perfused livers from normal rats and rats in various stages of development of dietary cirrhosis was studied. A choline-deficient, low-protein and high-fat diet was used. Results were obtained on oxygen consumption and carbon dioxide production, on glucose release and uptake by the liver and on changes in the concentrations of lactate and pyruvate and of beta-hydroxybutyrate and acetoacetate in the perfusion medium. 2. Oxygen consumption and carbon dioxide production were lower in fatty and cirrhotic livers than in normal livers. Ethanol had no effect on the oxygen consumption of any of the various livers. After addition of ethanol to the perfusion medium carbon dioxide production ceased almost completely in normal livers. Only a slight decrease in the carbon dioxide production occurred in fatty and cirrhotic livers. 3. With every type of liver glucose was released from the liver into the perfusion medium during the initial control period. This release continued after the addition of ethanol to the perfusion medium in experiments with normal and fatty livers, whereas with cirrhotic livers a marked uptake of glucose from the medium was found. A simultaneous release of the glycolytic end products lactate and pyruvate into the medium occurred. 4. The production of ketone bodies was equal in normal and early fatty livers (6 weeks on the fat diet). It was smaller in late fatty livers (3-4 months on the fatty diet) and in cirrhotic livers. 5. The lactate/pyruvate concentration ratio in the perfusion medium increased from 11 to 67 with normal livers, from 12 to 16 with early fatty livers, from 13 to 26 with late fatty livers and from 21 to 55 with cirrhotic livers when the livers were perfused with a medium containing ethanol. The beta-hydroxybutyrate/acetoacetate concentration ratio increased from 1.2 to 8.4 in normal livers, from 2.0 to 2.8 in early fatty livers, from 1.2 to 2.4 in late fatty livers and from 2.1 to 4.0 in cirrhotic livers when ethanol was added to the medium. 6. The effects of ethanol on liver metabolism during the development of dietary cirrhosis are discussed and related to human fatty liver and cirrhosis during chronic ethanol consumption.
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PMID:Influence of ethanol on the metabolism of perfused normal, fatty and cirrhotic rat livers. 596 89

The effect of ingestion of saline, glucose, and ethanol (isocaloric with the glucose) on the mobilization of radiopalmitate from epididymal fat prelabeled in vivo and the incorporation of the mobilized label into liver lipids was investigated in rats. The mobilization of radiopalmitate from epididymal fat and the incorporation of the mobilized label into liver triglyceride were most markedly elevated by ingestion of ethanol. Increased mobilization and diversion of epididymal adipose tissue fatty acids to liver lipids of ethanol-treated rats were shown also by the close resemblance of the fatty acids of liver triglyceride to the fatty acids of epididymal fat. The amount of radiopalmitate mobilized by the saline-treated rats, comprising approximately a third of that mobilized by the ethanol-treated animals, was larger than the amount mobilized by the rats treated with glucose; most of it was oxidized rather than incorporated into the liver fats. In glucose-treated rats a larger fraction of radiopalmitate mobilized from one prelabeled epididymal pad was diverted to and incorporated into the lipids of the contralateral pad of the same animal. The specific activity of hepatic triglyceride of ethanol- and saline-treated rats was similar and significantly higher than that of animals treated with glucose. These data indicate that the ethanol-induced fatty liver can be attributed to an increased mobilization and incorporation of adipose tissue fatty acids into liver lipid and to an altered hepatic metabolism of fatty acids and triglyceride.
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PMID:Effect of ingestion of saline, glucose, and ethanol on mobilization and hepatic incorporation of epididymal pad palmitate-1-14C in rats. 597 73

The effect of intestinal bacterial flora and endotoxin on fatty liver with germfree (GF) and conventional (CV) rat in the 12th and 24th week was investigated after giving fatty diet which was added 1% cholesterol-0.5% cholic acid to the basic diet. Results are as follows. Serum biochemistry Serum GOT, GPT, ALP and cholesterol values increased after giving the fatty diet in both groups. Limulus Gelation Test In CV group, endotoxin was detected in 2 of 10 cases in portal blood and was completely absent in arterial blood. After the fatty diet, endotoxin increased gradually both in portal and arterial blood. Cyclic AMP values on glucagon challenge (P/B ratio) In both groups, the levels of the P/B ratio maintained low values compared with control. In CV group, the values were lower in endotoxin positive cases than negative ones. Hepatic carbohydrate metabolism Abnormal hepatic F6P , glucose, FDP and PEP values were observed in CV group and reduction of the levels of hepatic F6P , G6P and glucose values were remarkable in GF group. Hepatic G6P in CV group and FDP in GF group remained unchanged. Impairment of F6P and G6P in CV group, was significant in endotoxin positive cases than in negative ones.
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PMID:[Pathogenesis of endogenous endotoxemia in chronic liver disease--with special reference to the experimental fatty liver in germfree animals]. 632 43

The role of glucose-6-phosphatase (G6Pase) in postreceptional glucose handling in non-insulin dependent diabetics ( NIDDs ) was in investigated by comparing the enzyme values in diagnostic liver biopsy samples with fasting blood glucose (BG), immunoreactive insulin (IRI) and plasma antipyrine half-life (T/2). The NIDDs , treated with sulphonylureas, had elevated serum aminotransferase and alkaline phosphatase values associated with fatty liver with or without fibrosis. G6Pase activity was reduced in the NIDDs compared with subjects who had undergone gallstone surgery (p less than 0.001), insulin dependent diabetics (p less than 0.001), and age- and sex-matched non-diabetics (p less than 0.001). G6Pase was inversely related to BG and antipyrine T/2, but not to IRI or conventional liver function tests. Therapy with phenobarbital and medroxyprogesterone acetate, known inducers, increased G6Pase activity, shortened antipyrine T/2, reduced BG and did not alter IRI, in four NIDDs . Low liver G6Pase activity in NIDDs may hence be one factor underlying the impaired glycemic control.
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PMID:Hepatic glucose-6-phosphatase activity in non-insulin dependent diabetics. Effect of enzyme-inducing drugs. 632 98

Insulin and C-peptide in venous blood were determined during oral glucose tolerance testing in 59 non-manifest diabetics with histologically established chronic liver disease (fatty degeneration, chronic aggressive hepatitis, cirrhosis). Glucose tolerance was pathologic in 60-80% of patients. When compared to a control group patients with chronic liver disease showed significantly increased values of blood glucose (after glucose intake), of insulin and of C-peptide (fasting and after glucose intake). The C-peptide/insulin ratio, a measure of hepatic insulin degradation, was significantly decreased after glucose uptake. There were no significant differences of blood sugar, insulin and C-peptide among the various liver diseases. In chronic aggressive hepatitis and in cirrhosis the C-peptide/insulin ratio was partly significantly lower than in fatty degeneration. From the increased C-peptide values increased insulin secretion in chronic liver diseases can be deducted. In addition, the decreased C-peptide/insulin ratios show an impairment of insulin degradation in liver cirrhosis and other chronic hepatic diseases. However, in fatty liver degeneration this is clearly less pronounced than in more serious liver diseases.
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PMID:[Insulin and C-peptide in chronic liver diseases during oral glucose tolerance testing]. 636 4

Metabolism of fat was studied in Sprague-Dowley rats receiving catecholamines as an experimental model of "stressed condition". These rats were fed with intravenous hyperalimentation with glucose only (G-group) or glucose and fat (F-group). Changes in body weight, cumulative nitrogen balance, blood sugar, serum IRI, free fatty acid, and triglyceride content of the liver were determined before and after five days intravenous hyperalimentation. Animals receiving intravenous hyperalimentation but no catecholamines were also subjected to the studies as control group. The following results were obtained from the present studies: In control group, G-group gained much more body weight and spared much more nitrogen than F-group. In catecholamine receiving groups, there was no significant difference of changes in body weight and cumulative nitrogen balance between G-group and F-group. In catecholamine receiving group, triglyceride content of the liver tissue was higher in G-group than in F-group, whereas triglyceride content of the liver tissue in control group was lower in G-group than in F-group. There was a positive correlation between the accumulation of triglyceride in the liver tissue and blood sugar level, or serum IRI level. A negative correlation was found between the accumulation of triglyceride in the liver tissue and plasma free fatty acid level. These results suggest that "stressed condition" induced by the administration of catecholamines enhanced the utilization of fat as an energy source without producing fatty liver.
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PMID:[Experimental studies on the effects of administration of catecholamines on fat metabolism]. 637 83


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