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

Adult female chickens were force-fed a corn-soy base diet at 150% of the daily amount consumed by those allowed the same diet ad libitum. Other hens were force-fed diets isocaloric to the 150% group just mentioned, but diet composition was adjusted so that 2/3 of the metabolizable energy (M.E.) came from the corn-soy diet and 1/3 from either corn oil or glucose; or force-fed a low energy diet accounting for 2/3 of the M.E. and corn oil 1/3 of M.E., or a purified diet accounting for all M.E. Fatty liver-hemorrhagic syndrome (FLHS) was induced in all force-fed groups with only the low energy diet plus corn oil having produced a significantly lower score for FLHS. However, the livers from the hens of the latter group had as much lipid, and the hens gained at least as much weight as those in other force-fed groups. During the third week of the experiment M.E. was determined along with a partition of energy among eggs, basal metabolism, body weight gain, and subsistance plus heat increment (H.I). The data showed that the hens force-fed corn oil had lower H.I. values indicative of associative dynamic action of fats at a plane of nutrition above normal. The data revealed that various types of diets and sources of energy in excess can induce FLHS, and this is discussed in terms of FLHS arising out of a positive energy balance.
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PMID:Various types of diets, sources of energy, and positive energy balance in the induction of fatty liver hemorrhagic syndrome. 93 96

To evaluate the role of insulin in familial hypertriglyceridemia, 34 relatives of the pedigrees of 3 index cases of endogenous hypertriglyceridemia and hepatic steatosis as well as 9 spouses were examined for plasma lipids and responses of blood glucose and plasma insulin during oral glucose tolerance tests. The combined disorders of hypertriglyceridemia and hyperinsulinemia plus glucose intolerance--insulin resistance--were most commonly found among the relatives, which were often accompanied by an impaired liver function. Some relatives showed hyperinsulinemia without hypertriglyceridemia. Obesity was frequent, but its incidence was similar to the controls. Thus, the observed form of familial hypertriglyceridemia was apparently coupled with insulin resistance; and hyperinsulinemia, or insulin resistance by itself, might be a basic genetical trait in this form of lipid disorder.
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PMID:Evidence for a familial form of hypertriglyceridemia as disorders coupled with insulin resistance. 96 Jan 7

Fatty liver and kidney syndrome, a disorder of young chicks, was studied under laboratory conditions. Affected chicks had enlarged livers (hepatomegaly), an increased content of lipid in the liver, and an increased level of palmitoleic acid in the liver lipids. The disorder was observed mainly in chicks from young parent flocks, and was associated either with commerical diets which were subsequently found to be low in biotin, or with specially formulated low-biotin diets. A third factor, imposition of stress, was required to initiate the disorder. There was evidence of increased lipogenesis causing an increase of triacylglycerols in the liver lipids and an increased production of saturated fatty acids, particularly palmitic acid. Increased levels of palmitoleic acid resulted from an increased desaturation of palmitic acid. Under stress, affected chicks had low blood glucose levels, suggesting that gluconeogenesis was impaired. Since biotin-dependent enzymes are involved in both gluconeogenesis and lipogenesis, it would appear that the relevant enzymes respond differently to a deficiency of biotin.
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PMID:Fatty liver and kidney syndrome in chicks. I. Effect of biotin in diet. 102 58

Among 31 nonobese or obese patients with endogenous hypertriglyceridemia, hepatic steatosis was found by histologic examination of the biopsied specimen in 17 patients, and it was severe in six patients, They had no history of excessive alcohol intake. Chemical analysis revealed that the lipid accumulated in the liver was triglyceride. The hypertriglyceridemic patients, with or without histologic steatosis, showed significantly increased responses of both plasma insulin and blood glucose to oral glucose load compared with control subjects. The responses were more exaggerated in the hypertriglyceridemic patients with steatosis than in the hypertriglyceridemic patients without steatosis. Analysis of correlations between five variables (liver triglyceride, plasma insulin, blood glucose, body weight index, and serum triglyceride) was done on 15 subjects whose liver triglyceride values were quantified, and highly significant correlations were found between liver triglyceride and plasma insulin, blood glucose, or body weight index. A step wise multiple regression analysis performed on the five variables with liver triglyceride as the dependent variable revealed that the plasma insulin level was the most closely related variable, and the blood glucose level the next. The prediction equation for liver triglyceride as a function of plasma insulin and blood glucose levels (r = 0.91, p greater than 0.001) accounted for 84 percent of the total variance of liver triglyceride. It was shown that the decay of intravenously injected insulin in plasma was not delayed in the hypertriglyceridemic patients with steatosis, while the insulin sensitivity examined after intravenous insulin injection significantly decreased in the hypertriglyceridemic patients with or without steatosis, thus suggesting that the hyperinsulinemia in the hypertriglyceridemic patients was due to an increased insulin secretion associated with the decrease in the insulin sensitivity. Therefore, the elevated plasma insulin and blood glucose levels--or the insulin insensitivity by itself--might be the essential abnormalities in patients with endogenous hypertriglyceridemia, which, in extreme cases, might lead to massive triglyceride accumulation in the liver.
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PMID:Hepatic steatosis and the elevated plasma insulin level in patients with endogenous hypertriglyceridemia. 112 34

Chicks with fatty liver and kidney syndrome (FLKS) were given oral doses of one of the following test solutions: water, glucose, maltose, starch. Plasma glucose concentration was measured during the four subsequent hours. All FLKS-affected chicks were hypoglycaemic before treatment. Although in some cases plasma glucose concentration increased slightly in the FLSK-chicks given water alone, significantly greater increases were invariably observed following the administration of carbohydrate to sick birds. Results obtained from dietary experiments in which starch was replaced by glucose in a ration causing high mortality from the syndrome revealed no beneficial effect due to the substitution. It was concluded that FLKS does not involve any major impairmant of carbohydrate digestion or absorption.
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PMID:Carbohydrate absorption by chicks affected with the fatty liver and kidney syndrome. 115 1

Marked fatty liver was found to develop in both KK and KK-Ay (yellow KK) mice when they were allowed free access to a 15% ethanol solution as drinking fluid. The present studies were undertaken to elucidate the characterization of the fatty liver and associated changes. Chemical analysis showed that accumulated lipids were mainly triglycerides, whose fatty acid composition was changed with increases in palmitoleic and oleic acids, indicating augmentation in endogenous lipogenesis. An accumulation of small fat droplets was histologically observed in centrolobular hepatocytes extending to perilobular zones. Among the tested mice of seven strains, only KK and KK-Ay mice developed the ethanol-induced fatty liver, and the latter mice were more susceptible. Growth, food and alcohol intakes, plasma levels of glucose, triglycerides, and immunoreactive insulin were also surveyed during the development of the alcoholic fatty liver. In contrast to high energy diet, ethanol induced neither development of obesity nor exaggeration of diabetic states. A possible correlation between the pathogenesis of the fatty liver and the genetic factor inherited in KK mice is discussed.
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PMID:Induction of fatty liver by ethanol drinking in KK and KK-Ay mice. 115 19

The effect of physical training and exhaustive exercise on fatty acid synthesis in rat liver and adipose tissue has been investigated. Exercise training (treadmill running) significantly (p less than 0.05) decreased body wt, eipdidymal fat pad wt, adipocyte size, and hepatic fatty acid synthetase activity. Training did not significantly affect adipose tissue cell number, lipogenesis from glucose-U-14C, or fatty acid synthetase. Exercise to exhaustion immediately prior to sacrifice significantly (p less than 0.05) decreased lipogenesis from glucose-U-14C and fatty acid synthetase in adipose tissue from trained but not untrained rats. Liver fatty acid synthetase was not significantly influenced by exhaustive exercise. The results of this study indicate that rats may adapt to physical training by decreasing adipose tissue lipogenesis during exhaustive exercise. This adaptation in energy metabolism may facilitate physically trained animals in conserving blood glucose during exhaustive exercise, thereby prolonging endurance.
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PMID:Response of lipogenesis and fatty acid synthetase to physical training and exhaustive exercise in rats. 116 May 24

Young, adult, female Sprague-Dawley rats were fasted for 18 h and then given a single s.c. injection of alloxan (10 mg/100 g body weight) which promptly induced a severe state of diabetes. The animals were killed at frequent time intervals during the 7-day study period in order to record the dynamic changes in their capacity for adrenal steroidogenesis and secretion as measured by fluorometric determination of their circulating corticosterone (Cmpd B) levels as well as by thin layer chromatographic identification of cortical lipid moieties used for steroidogenesis. In addition to severe polydypsia, polyuria and polyphagia, these animals manifested super-normal glucose, triglycerides, free fatty acids and cholesterol in their blood, severe hepatic steatosis, adrenal hyperplasia with lipid depletion from the mineralocorticoid producing z. glomerulosa, thymus gland involution and complete degranulation of their insulin producing islet beta cells. Despite an initial high output of Cmpd B and despite progressive cortical hyperplasia, the serum Cmpd B levels became reduced and many of the animals succumbed suddenly, due most likely to inadequate adrenocortical steroidogenesis. Adrenocortical lipids showed a progressive accumulation of free fatty acids, di- and triglycerides, suggesting that some lipid enzymatic defect could be responsible for the lack of conversion of these lipid entities essential for proper steroidogenesis.
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PMID:Adrenal glandular lipids and circulating corticosterone in severely diabetic rats. 117 54

1. The occurence of biotin deficiency and fatty liver and kidney syndrome (FLKS) in chicks was studied using a 2x2x2x2 factorial-design experiment in which the variables were dietary biotin, fat and protein, and starvation. 2. The severity of biotin deficiency, using growth retardation and severity of dermal lesions as criteria, was least when the low-biotin diet also contained low levels of fat and protein. Addition of fat or protein increased the severity of the deficiency. Tissue fatty acid composition was affected by biotin deficiency only in those birds given the low-protein, low-fat diet. The main change was an increase in the ratio, 16:1 fatty acids :18:0 fatty acids. Plasma glucose and free fatty acid levels in non-fasted birds were unaffected by the dietary variables. 3. Mortality from FLKS with the diet containing low biotin, fat and protein levels was 52% at 28d, but was reduced or eliminated when the dietary level of any of these ingredients was increased. 4. Starvation considerably increased the incidnece of FLKS in the period immediately after fasting, and also affected plasma glucose and free fatty acid concentrations. Liver fatty acid composition, indicated an increase in the proportion of 18:0 at the expense of 16:1 and concentrations increased in proportion, at the expense of 18:0. 5. The relationship between biotin deficiency and FLKS, and a possible mechanism for the induction of FLKS by starvation are discussed.
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PMID:Biotin deficiency and fatty liver and kidney syndrome in chicks given purified diets containing different fat and protein levels. 124 38

Two trials were to study alloxan diabetes in goats. The data were grouped: 1) normal fed goats (10); 2) 48-h fasted goats (5); 3) fed goats sampled 96 h after alloxan treatment (5); and 4) goats treated with alloxan following a 48-h fast and sampled 96 h after alloxan treatment with continued fasting (3). Groups 1 and 4 exhibited the following means: serum insulin 43.9, 16.4, 9.4, and 6.7 muU/ml; blood glucose 55.0, 47.3, 219.6, and 485.6 mg/100 ml; blood ketones 4.3, 2.6, 36.6, and 28.6 mg/100 ml; blood acetate 4.7, 4.0, 42.7, and 4.9 mg/100 ml; plasma-free fatty acids 1.8, 10.0, 14.4, and 40.5 mg/100 ml; and plasma triglyceride 13.3, 7.0, 47.6, and 12.2 mg/100 ml. Liver samples from five fed goats before and 12 days after alloxan treatment exhibited the following means: phospholipid 27.5 and 26.1 mg/g; triglyceride 21.2 and 98.9 mg/g; and percent lipid 7.2 and 14.4. The diabetes was accompanied by fatty liver development and probably reduction in utilization of acetate and triglyceride in the fed animals.
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PMID:Blood and liver metabolites in fed and fasted diabetic goats. 124 92


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