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

The role of biotin-dependent enzymes in the fatty liver and kidney syndrome of young chicks was studied. Under conditions of a marginal deficiency of dietary biotin, the level of biotin in the liver has differing effects on the activities of two biotin-dependent enzymes, pyruvate carboxylase and acetyl-CoA carboxylase. The activity of acetyl-CoA carboxylase is increased, but when the dietary deficiency of biotin produces biotin levels which are below 0-8 mug/g of liver, the activity of pyruvate carboxylase may be insufficient to completely metabolize pyruvate via gluconeogenesis. There is an increase in liver size and in the activities of enzymes involved in alternate pathways for the removal of pyruvate. Blood lactate accumulates and there is increased synthesis of fatty acids, and an accumulation of palmitoleic acid; these steps are accomplished by increased activities of at least the following enzymes: acetyl-CoA carboxylase, malate dehydrogenase (decarboxylating) (NADP+) and the desaturase enzyme. When the biotin level is below 0-35 mug/g of liver and the chick is subjected to a stress, physiological defence mechanisms of the chick may be inadequate to maintain homeostasis and they finally collapse, resulting in accumulation of triacylglycerol in the liver and blood; the chick is unable to maintain blood glucose levels and death occurs, often only a few hours after the imposition of the stress.
Aust J Biol Sci 1976 Dec
PMID:Fatty liver and kidney syndrome in chicks. II. Biochemical role of biotin. 1 36

Alcoholic hyalin was found in liver of a nonalcoholic patient with fatty liver after long-term glucocorticoid therapy for systemic lupus erythematosus. Hepatocytes including hyalin bodies showed fatty change or vesiculated degeneration. Occasionally, basophilic substance which was recognized in the hepatocytes with or without hyalin was noticed showing the feature quite similar to delicate alcoholic hyalin.
Acta Hepatogastroenterol (Stuttg) 1977 Dec
PMID:Nonalcoholic fatty liver with alcoholic hyalin after long-term glucocorticoid therapy. 7 31

Isopropanol and acetone administered to rats in conditions leading to a similar blood acetone level differ markedly in their effects on lipid metabolism. Isopropanol administration determines a fatty liver, which is mainly related to a defect in hepatic lipoprotein synthesis. Acetone administration gives only raise to a slight increase in the liver triacylglycerol level. It does not alter the [1-14C] palmitate, [1-14C] glycerol or [U-14C] leucine incorporation into blood lipoproteins. Acetone does thus not appear to play a preminent role in the isopropanol induced fatty liver which seems to be related mainly to a direct action of the alcohol itself.
Arch Int Physiol Biochim 1977 Dec
PMID:[Comparison of the effect of acetone and isopropanol on lipid metabolism in rats]. 7 72

The effect of carbon-tetrachloride poisoning and the protection caused by AMP were studied. A single dose of CCl4 has resulted in a rapid development of a fatty liver, a considerable increase in serum enzymes, glutamic oxalacetic and pyruvic transaminases as well as serum-alkaline phosphatase. Total serum protein showed a tendency to decrease accompanied by a decrease in A/G ratio. Administration of adenosine-5-monophosphate prevented the increase in serum-alkaline phosphatase and increased the A/G ratio. There was, however, a slight but significant decrease in serum GOT and GPT within the 24-hrs. period of study, but it remained still higher than that of the control. AMP lowered liver fat without complete protection against the development of fatty liver.
Z Ernahrungswiss 1977 Dec
PMID:Effect of AMP on acute carbon-tetrachloride hepatotoxicity. 20 15

Indirect calorimetric studies were performed during a 100 g oral glucose tolerance test in diabetic patients with varying degrees of endocrine pancreatic dysfunction and in a control group of normal subjects. In 3 obese diabetics the study was repeated after a 3 day protein sparing modiefied fast. In diabetic patients the results show alterations of oxidation and storage of carbohydrates, related to insulin secretion deficiency on the one hand, and to overweight on the other. Endocrine pancreatic insufficiency may account directly for alterations observed in individuals with decreased or absent insulin response to glucose load, wheras metabolic factors such as adipose mass, hepatic steatosis, and peripheral insulin resistance appear to be responsible for alterations in carbohydrate oxidation and storage in subjects with relative endocrine pancreatic insufficiency, particularly obese diabetics.
Schweiz Med Wochenschr 1979 Dec 01
PMID:[Changes in storage and oxydation of ingested glucose in obesity and diabetes mellitus]. 51 18

It has been postulated in recent years that idiopathic necrosis of the head of the femur may possibly be caused by arteriolar obstruction by fat emboli emanating from a fatty liver, which would act as a reservoir, due to various causes such as alcoholism and prolonged steroid therapy. A similar situation has been found in human pathology in post traumatic fat embolism. The writers have reviewed forty five cases of post traumatic fat embolism which had passed the pulmonary filter. All the cases were reviewed after a minimum of two years, since this is considered the minimum time within which necrosis can manifest itself radiologically. In none of these cases was there any evidence of necrosis of the head of the femur. These findings, supported by other critical considerations. do not lend support to the theory of fat embolism as a case of idiopathic bone necrosis.
Ital J Orthop Traumatol 1979 Dec
PMID:Fat embolism as a cause of idiopathic necrosis of the head of the femur. Review of forty five cases of post traumatic fat embolism. 55 16

The metabolism of varying quantities of oleic acid was examined in isolated perfused livers from normal fed rats and from animals made diabetic by pretreatment with guinea pig antiinsulin serum (AIS). The data presented reemphasize the fact that the quantity of free fatty acid (FFA) coming to the liver is a necessary, but not the most important, factor affecting the subsequent metabolism of the FFA. Rates of ketogenesis and output of triglyceride and the terminal concentration of hepatic triglyceride were proportional to uptake of FFA in certain concentration ranges. For equal rates of uptake of FFA, ketogenesis was greater, and the quantity of triglyceride secreted or accumulated within the liver was less, with livers from diabetic animals than with livers from normal animals. In confirmation of previous data, the liver was observed to have a maximal capacity to secrete triglyceride. Triglyceride accumulated in livers from normal-fed and diabetic animals only when uptake of FFA was more than sufficient to saturate the secretory process. Since proportionately more FFA was catabolized by livers from AIS treated animals, greater uptake of FFA was required to produce maximal rates of output of triglyceride and accumulation in livers from diabetic than from normal animals. Rates of ketogenesis by livers from normal fed animals increased minimally with increasing uptake of FFA (up to 1.0 mM free fatty acid). Even when uptake increased considerably with FFA concentrations of approximately 2.5 mM, rates of ketogenesis by livers from normal animals were less than half those of livers from diabetic rats, and maximal rates were not achieved by the normal controls. It is evident that changes in hepatic metabolism of FFA in the intact diabetic animal result from simultaneous alterations of supply of FFA and hormonally induced metabolic changes in the liver. Moreover, although hepatic secretion and accumulation of triglyceride is greater in isolated perfused livers from normal rats than from diabetic animals when the livers are exposed to equal quantities of FFA, the diabetic livers can accumulate more triglyceride, secrete more triglyceride, and oxidize more FFA to ketone bodies than can the normal under conditions in which considerably more substrate is available to the diabetic rather than to the normal livers. These differences might also be expected to occur in the acutely insulin deficient intact animal, in which changes in hormonal status and substrate (FFA) availability occur simultaneously, and might, in part, explain the ketonemia, hypertriglyceridemia, and hepatic steatosis often observed in vivo.
Metabolism 1978 Dec
PMID:The metabolism of oleic acid by the perfused rat liver in experimental diabetes induced by antiinsulin serum. 72 30

The relationship between Reye-Johnson syndrome and acute encephalopathy without fatty liver was investigated by comparing the lipid composition of liver samples obtained from five patients with Reye-Johnson syndrome, two patients with acute encephalopathy, and five controls. The mean total hepatic triglyceride concentration was increased nearly sevenfold in Reye-Johnson syndrome and slightly decreased in acute encephalopathy when compared with the mean control value. The mean total hepatic free fatty acid concentration was increased nearly threefold in acute encephalopathy when compared with the mean value in Reye-Johnson syndrome. Total phospholipid content was decreased in the liver in Reye-Johnson syndrome, and this difference was caused mainly by a diminution of the hepatic lecithin fraction. The ratio of palmitic acid to oleic acid and hepatic free fatty acids was 2.5 in Reye-Johnson syndrome, 0.7 in acute encephalopathy, and 0.8 in controls. These results suggest that, despite clinical similarities and laboratory evidence of hepatic dysfunction in both Reye-Johnson syndrome and acute encephalopathy, different pathogenic mechanisms may be responsible for the liver abnormalities found in the two syndromes.
Mayo Clin Proc 1976 Dec
PMID:Hepatic lipids in Reye-Johnson syndrome and in acute encephalopathy without fatty liver. 99 54

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.
Aust J Biol Sci 1976 Dec
PMID:Fatty liver and kidney syndrome in chicks. I. Effect of biotin in diet. 102 58

The in vitro and in vivo incorporation of (2-14C)acetate into lipids of mink (Mustela vison) liver and intestines was studied. In vitro, a dose of aflatoxin B1 as small as 7.5 mug/ml of medium reduced by 20% the amount of (2-14C)acetate incorporated into lipids of mink liver slices, whereas 180 mug caused 76% reduction in the synthesis of lipids from the radioactive precusor. Similar inhibition of lipid synthesis by aflatoxin also was observed with tissues from mink intestines and fatty liver. The degree of inhibition (19 to 84% for tissue from intestines and 19 to 64% for tissue from fatty livers) depended on the amount of aflatoxin B1 (7.5 TO 180 MUG) present in the medium. In vivo, a substantially increased amount of 14C-labeled lipids was found in the livers of mink injected with 600 mug of aflatoxin B1 per kg of body weight 20, 28, and 40 h earlier. However, no appreciable difference in incorporation of (2-14C)acetate into lipids was observed between toxin-treated and control animals when these animals were sacrificed and examined for 14C-labeled lipids at 4 and 10 h after toxin was administered.
Appl Microbiol 1975 Dec
PMID:Incorporation of (2-14C)acetate into lipids of mink (Mustela vison) liver and intestine during in vitro and in vivo treatment with aflatoxin B1. 121 38


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