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

Splanchnic metabolism was studied to quantify changes underlying the fatty liver, hyperlipemia, and hypoglycemia produced by ethanol. Four subjects fasted for 15 h were compared with five subjects fasted for 69 h under basal conditions and during continuous intravenous infusion of sufficient ethanol to give a concentration of 3-5 mM in arterial blood plasma. Splanchnic storage of fatty acids was estimated from the difference between uptake of FFA and secretion of derived products. Basal values for splanchnic uptake of FFA were twofold higher after the 69-h fast while splanchnic storage of fatty acids and production of ketone bodies increased threefold. Values for basal secreation into the blood of triglycerides derived from FFA were similar in the two groups. In both nutritional states, the fraction of FFA taken up in the splanchnic region oxidized to ketone bodies and to CO2 fell when ethanol was given because of preferential oxidation of ethanol to acetate, and the fraction esterified rose. However, systemic transport and splanchnic uptake of FFA fell with ethanol in subjects fasted 15 h, so that neither storage of triglycerides in splanchnic tissues nor secretion into the blood increased. In subjects fasted 69 h, ethanol increased transport of FFA and splanchnic storage of fat. In all but one subject it also increased secretion of triglycerides into the blood. The concentration of glucose in blood fell during ethanol infusion in all five subjects undergoing the 69-h fast. Mean splanchnic glucose production was maintained at about one-half of the pre-ethanol value, despite virtual cessation of splanchnic uptake of lactate and of those amino acids that are metabolized via malate. Quantitative estimates of extrasplanchnic metabolism suggest that enhanced formation of alpha-glycerophosphate from glucose, in addition to impaired hepatic gluconeogenesis, may contribute to ethanol-induced hypoglycemia in man.
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PMID:Effects of a 3-day fast and of ethanol on splanchnic metabolism of FFA, amino acids, and carbohydrates in healthy young men. 17 79

A 47-year-old man who had cerebellar ataxia and low plasma lipid and lipoprotein levels is reported. His tendon reflexes were hyperactive and the plantar responses were extensor. There was no acanthocytosis. Total lipids (380 mg/dl), total cholesterol (106 mg/dl), esterified cholesterol (74 mg/dl), triglyceride (58 mg/dl), phospholipids (124 mg/dl) and free fatty acids (303 muequiv./l) were generally decreased. A disturbance of lipid absorption due to a defect of chylomicron formation and hepatic steatosis were also disclosed. On lipoprotein electrophoresis, prebetalipoprotein was very faint and migrated more slowly than normal. Betalipoprotein and alphalipoprotein were moderately reduced in concentration but migrated normally. The concentration of isolated VLDL was only one-tenth of that in normal subjects and it migrated as slow prebetalipoprotein. Although the lipid composition of VLDL was similar to that of normal VLDL, the lack of minor components was disclosed by SDS-PAG electrophoresis. Incorporation of [1-14C]acetate into VLDL lipids was significantly reduced to a greater extent than that of LDL and HDL. From these findings, we discuss the possibility that hypobetalipoproteinemia results from impaired VLDL synthesis.
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PMID:Hypobetalipoproteinemia with abnormal prebetalipoprotein. 19 71

In vitro hepatic synthesis of lipids starting from 1-(14)C-acetate was studied in rats made diabetic by subcutaneous alloxan administration (175 mg/kg b.w.). A second group of diabetic rats was treated with lente insulin. In the alloxan-treated rats, a decrese was observed in hepatic incorporation of 1-(14)C-acetate into phospholipids, triglycerides and esterified cholesterol; there was an increased incorporation into nonesterified fatty acids (NEFA) and free cholesterol. Insulin administration restored lipid synthesis values to normal. On histologic examination, an intranuclear glycogenesis was observed in the hepatocytes of the alloxan-treated rats, along with severe hepatic necrosis; the latter however, only in rats sacrified on the 3rd day. Hepatic steatosis with small, medium and large droplets was present in the insulin-treated rats; signs of cellular degeneration were less evident.
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PMID:Effects of insulin on hepatic lipid synthesis in alloxan diabetic rats. 39 74

An overview of dermatological diseases which occur in conjunction with oral contraceptive (o.c.) use is presented. An increase in pigmentation during o.c. use is attributed to an increase in the binding of cortisol with transcortin caused by the estrogen component, which leads to an increase in melanin-stimulating hormone production. Sebum production is decreased during o.c. use, which has a beneficial effect in cases of acne and seborrhea oleosa. This effect is most pronounced with preparations containing chlormadinon acetate, which has an antiandrogenic effect. O.C. use can influence hair growth by disturbing the balance between anagenic and telogenic hairs. Androgenetic alopecia is most often caused by preparations containing nortestosterone. Peroral dermatitits, lupus erythmatodes visceralis and similar disorders, and allergic skin reactions have been observed among o.c. users. Porphyria cutanea tarda is generally found in young women in conjunction with o.c. use, which can be related to liver dysfunctions. Vaginal candidosis is also more frequently found among o.c. users, particularly in conjunction with combination preparations. Herpes gestationes can occur during o.c. use, mainly among women who developed it during pregnancy. Progesterone appears to be responsible for provoking the condition. 166 patients who developed dermatological disorders during o.c. use were studied according to the preparation each used. Acne vulgaris improved more frequently among Ovosiston users. A marked increase in vaginal fluor indicated an increase in trichomoniasis and candida mycosis. In all observed cases of porphyria cutanea tarda, liver damage (hepatitis, cyrrhosis, or fatty liver) could be ascertained.
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PMID:[Reactions and side effects of ovulation inhibitors on the skin]. 72 69

Vitamin A is normally transported in plasma as retinol bound to a specific protein, retinol-binding protein (RBP). Detailed studies were conducted to examine the effects of excess vitamin A on the plasma concentration and metabolism of RBP, and to obtain information about vitamin A transport in the hypervitaminotic state. Two separate experiments were conducted. In the first (Study I, 99 days), plasma RBP and vitamin A levels were compared in three groups of rats fed 0.14 mg (control), 7.3 mg (group 2), or 41 mg (group 3) of vitamin A per day. After day 50 of the study, the administration of excess vitamin A to hypervitaminotic rats (groups 2 and 3) was discontinued and the rats were allowed to recover from vitamin A toxicity. In the second, shorter experiment (Study II), serum vitamin A and RBP levels were compared in control and hypervitaminotic (34 mg of retinyl acetate per day) rats. The rats in this study were also given [3-H]retinyl acetate daily to determine the distribution of retinyl esters and retinol between the lipoprotein and nonlipoprotein protein fractions of plasma. In both studies, administration of large, excessive doses of vitamin A resulted in substantial and significant decreases in the levels of serum RBP. Excessive doses of vitamin A produced fatty liver in the rats, in association with a normal (group 2, Study I) or with a decreased (group 3, Study I) level of RBP in the liver. It is possible that excess vitamin A leads to decreased rates of RBP synthesis in, and of RBP secretion from, the liver. Administration of excessive doses of vitamin A also resulted in elevations of serum vitamin A levels, which were mainly due to large increases in the circulating levels of retinyl esters. In the hypervitaminotic rats, most of the serum vitamin A, and virtually all of the retinyl esters, was found in association with the serum lipoproteins of hydrated density less than 1.21. These results demonstrate that the serum lipoproteins play an important role in the transport of the vitamin A that accumulates in serum in hypervitaminosis A. We suggest that the toxic manifestations of hypervitaminosis A occur when vitamin A circulates in plasma and is presented to membranes in a form other than bound to RBP. Plasma lipoproteins may nonspecificially deliver vitamin A to biological membranes and hence lead to vitamin A toxicity.
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PMID:Metabolism of retinol-binding protein and vitamin A during hypervitaminosis A in the rat. 112 57

To study possible factors in the pathogenesis of the ethanol-induced fatty liver, we investigated the effect of chronic ethanol consumption on the metabolism of fatty acids by isolated hepatic mitochondria. Chronic ethanol consumption resulted in decreased fatty acid oxidation, as evidenced by a reduction in oxygen uptake and CO2 production associated with the oxidation of fatty acids. The State 3 rate of oxygen uptake was depressed to a greater extent than the State 4 or the uncoupler-stimulated rate; the respiratory control ratio was also decreased. Therefore, one site of action of chronic ethanol feeding is on oxidative phosphorylation. The reduction in fatty acid oxidation, in general, is not due to an effect on the activation or translocation of fatty acids into the mitochondria. There was no effect by ethanol feeding on the activity of palmitoyl coenzyme A synthetase, whereas carnitine palmitoyltransferase activity was increased. The use of an artificial system (formazan production) to study beta oxidation in the absence of the electron transport chain is described. In the presence of fluorocitrate, which inhibits citric acid cycle activity, ketogenesis and formazan production were increased by chronic ethanol consumption. Thus beta oxidation to the level of acetyl-CoA is not impaired by chronic ethanol consumption. Total oxidation of fatty acids to CO2 is depressed by chronic ethanol intoxication because of effects on oxidative phosphorylation or the citric acid cycle (or both). Neither nutritional deficiency, cofactor depletion, nor the presence of ethanol in vitro explains these effects. Several of the effects of chronic ethanol consumption on fatty acid oxidation are mimicked by acetaldehyde and acetate, products of ethanol oxidation. Chronic ethanol consumption leads to persistent impairment of mitochondrial oxidation of fatty acids to CO2. However, oxidation of fatty acids to acetyl-CoA is not decreased by chronic ethanol consumption.
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PMID:Effect of chronic ethanol ingestion on fatty acid oxidation by hepatic mitochondria. 117 Oct 98

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.
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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

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

Previous research has shown that a combination of feed restriction and dietary 1,3-butanediol starting at 14 d post-partum resulted in fatty liver and ketosis. Sixteen multiparous Holstein cows were used to determine effects of feed restriction or 1,3-butanediol as separate treatments. Treatments during d 14 to 42 postpartum were 1) control (ad libitum intake), 2) 20% feed restriction, or 3) control plus dietary 1,3-butanediol (5.5% of DM). From d 43 to 56, cows assigned to treatments 2 and 3 received a combination of feed restriction and butanediol. One cow on treatment 2 developed ketosis, but not fatty liver, after only 4 d of feed restriction. No other cows developed fatty liver or ketosis. Both treatments decreased milk production compared with controls. Feed restriction increased the extent of negative energy balance and caused transient increases in concentrations of NEFA, acetate, and beta-hydroxybutyrate in plasma. Concentrations of beta-hydroxybutyrate and insulin in plasma were increased by butanediol, which is a potent ketone body precursor. Concentration of glycogen in liver was less in feed-restricted cows, whereas glycogen and total lipid were greater in cows given butanediol separately. Gluconeogenic capacity of liver slices was not different among groups. Addition of 1,3-butanediol to in vitro incubation media decreased oxidation of propionate to CO2. Neither feed restriction nor dietary 1,3-butanediol as separate treatments induced the fatty liver and ketosis observed in earlier experiments in which the two treatments were given together.
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PMID:Metabolic changes in blood and liver of dairy cows during either feed restriction or administration of 1,3-butanediol. 178 95

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


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