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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

In order to clarify the mechanism of alcoholic fatty liver, rats were reared with alcohol diet from adult, foetal or weanling periods. When rats were fed with the diet from adult for 4 weeks, these livers showed apparent fatty deposition histologically and biochemically. Low density lipoprotein (LDL) in serums of these rats lowered in level significantly than control, which indicate decreased production of secretion of very low density lipoprotein (VLDL) in the liver from which converted to LDL in peripheral tissues. When rats were reared with the diet from their foetal life, their livers deposited little of fat at any time examined after birth up to 13 weeks in spite of good diet uptake. The same phenomenon was observed in rats reared from their weanling period with the diet. In situ liver perfusion was performed to clarify the anti-fatty liver mechanism. Ketone body (KB) production rates from palmitate infused constantly at physiological concentration and bile production rates were not different among control, weanling and foetal groups. Oxygen consumption rate in control decreased after infusion of palmitate-albumin complex solution. However the rates in weanling and foetal alcohol rats increased significantly after infusion of the solution. The latter group showed more increase in rate than the former. When theoretical oxygen consumption for production of KB was compared with actual one, livers from control rats seemed to use the whole oxygen for KB production. On the other hand only 59.7% of whole oxygen in foetal alcohol group and 85.9% in weanling group used for KB production respectively. It is surmized that the increased non ketone oxygen in these groups, especially in foetal alcohol group, indicate the anti-fatty liver mechanism in these groups, probably augmented FFA oxidation. Electrophoretic analysis of lipoproteins in chronic alcoholisms showed decreased beta and pre-beta band and increased alpha band. These changes returned to normal after 1 week of admission. These experimental and clinical data indicate that impaired oxidation of FFA is an important factor for the formation of alcoholic fatty liver and impaired transport of fat from liver might enhance the change in the liver.
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PMID:[Experimental and clinical studies on the mechanism of alcoholic fatty liver (author's transl)]. 54 10

The fatty liver often found in untreated kwashiorkor has been associated with highly variable concentration of circulating lipids. The effect on lipid metabolism of two isocaloric diets--one synthetic monomolecular (Vivonex) and one standard (Casilan)--which both initiated satisfactory clinical improvement was studied in 21 Ethiopian children with kwashiorkor during the first weeks of rehabilitation. Before treatment mean fasting values of all biochemical parameters were within normal ranges except for moderately elevated triglycerides--an unexpected finding-and low insulin. Individual values varied greatly; triglyceride between 0.39 and 3.49 mmol/1. FFA correlated both to glycerol, D-beta-hydroxybutyrate and triglyceride values. During treatment insulin, glucose and glycerol remained essentially unchanged and were similar in both dietary groups. In the Vivonex group only there was an initial marked, parallel fall of FFA and D-beta-hydroxybutyrate suggesting greater availability of carbohydrate and enhanced glucose utilization. This pattern of response seemed to occur without comparable inhibition of lipolysis. Triglycerides--like serum albumin--increased faster in the Casilan group. The highest mean triglyceride value was reached by day 8 in the Casilan group and by day 15 in the Vivonex group. Ten minutes following heparin injection triglycerides declined, FFA and glycerol increased indicating release of in vivo active lipase. LPL activity assayed in vitro was similar and unaffected by 2 weeks of dietary treatment in both groups. LPL activity was inversely correlated to triglycerides providing--beside the type of diet--another possible explanation for the wide variations seen in circulatory triglycerides.
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PMID:Dietary effects in the early recovery phase of kwashiorkor. Plasma levels of triglycerides, FFA, D-beta-hydroxybutyrate, glycerol, postheparin lipoprotein lipase (LPL), glucose and insulin. 127 67

Three groups of freshly calved dairy cows suffering from fatty liver syndrome of different stages were examined for serum cholic acid (SCA) levels to assess the value of SCA-determination as a diagnostic approach to fatty liver syndrome. A. Comparison of the SCS levels between cows with and without ketonuria: Cows with ketonuria (n = 13) and with elevated plasma ASAT activity, indicating a moderate liver damage, showed a rise of their mean SCA level to 35.3 (+/- 14.9) mumol/l. Freshly calved cows without ketonuria (n = 10) had at the same time a mean SCA level of 17.9 (+/- 6.4) mumol/l, falling practically into the physiological range. The SCA level increased above the physiological range in 10 of the 13 cases with ketonuria, in seven of them even more than twice. B. Interrelationship between SCA level and hepatic lipid content: Increase in hepatic total lipid (TL) was always associated with SCA-elevation. The mean SCA level was 55 (+/- 22.0) mumol/l in cases of severe fatty liver (TL = 200-280 g/kg), and 39.5 (+/- 6.0) mumol/l in the moderate form (TL = 180-200 g/kg) of the syndrome. C. Peripartal SCA levels of cows with fatty liver: Clinically healthy cows (n = 6) with ketonuria and an elevation of serum ASAT and FFA concentrations had a mean SCA level of 35-45 mumol/l. One cow of this group, which developed acute fatty liver syndrome and died within the period of study, showed an extreme SCA level of 100 mumol/l in it's terminal stage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cholic acid levels in the serum of dairy cows with metabolically-caused liver diseases]. 204 69

Two trials were conducted to determine if estrogen contributes to development of fatty liver in dairy cattle. During trial 1, eight late lactation, nonpregnant cows were assigned to 0 or 15 mg estradiol-17 beta benzoate/d treatment. Days 1 to 3 of the trial were for baseline measurements, and treatments were given from d 4 to 21; on d 20 and 21 animals were fasted. Short-term feed deprivation resulted in increased plasma FFA concentrations and rapid accumulation of triglyceride into liver tissue obtained by biopsy. During starvation, plasma FFA concentration and liver triglyceride content were lower for cows receiving the estradiol-17 beta treatment relative to cows receiving control treatment. Very low density lipoprotein concentration in blood increased dramatically in three of four animals during estradiol-17 beta administration. Because of the decrease in milk production during estradiol-17 beta treatment, it was not known whether this represented a decrease in very low density lipoprotein clearance from blood or reflected a lipotropic response to estradiol-17 beta. Therefore, a second trial was conducted employing nonlactating cows, and control and estradiol-17 beta-treated animals were pair fed. The trial was 33 d with d 1 to 3 for baseline measurements, and treatments were administered from d 4 to 33. All animals were starved from d 19 to 23. Estradiol-17 beta increased hepatic lipid and triglyceride accumulation and plasma very low density lipoprotein concentration during starvation. Plasma FFA concentration was also increased by estradiol-17 beta during this time; therefore, a direct or indirect effect of estrogen on hepatic lipid metabolism could not be delineated.
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PMID:Estrogen induction of fatty liver in dairy cattle. 238 18

Free fatty acids, cholesterol and phospholipids in plasma were studied from 6 weeks before to 6 weeks after calving in 16 normal multiparous cows. The same plasma lipids were studied the day after calving in 20 normal primiparous cows. Ten of these were fed according to standards and the other 10 were overfed the last 3 weeks prepartum. The plasma lipids were also analysed in 16 cows with left displacement of the abomasum and fatty liver, and in 16 cows with ketosis with no or only slight fat infiltration of the liver. In the normal cows there was a rise in FFA-level and a reduction in cholesterol and phospholipids from 6 weeks before to the day after calving. Thereafter there was a reduction of FFA-level and rise in cholesterol and phospholipids. Increased feed intensity had no effect on plasma lipids at calving. The level of the plasma lipids in cows with fatty liver differed very much from the amounts in normal cows at corresponding time from calving. Cows with ketosis had high FFA-level but the amount of cholesterol and phospholipids differed very little from normal cows.
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PMID:Plasma lipids in normal cows around partus and in cows with metabolic disorders with and without fatty liver. 264 Jul 81

Recently numerous reports show deleterious effects of alcohol abuse on pregnant women giving their children a high risk of stillbirth and/or several developmental abnormalities and mental retardation, i.e. the Fetal alcohol syndrome (FAS). In the present study, the effects of maternal alcohol consumption on lipid metabolism in the litter liver were investigated in rats. These rats showed not only quite less lipid deposition in spite of large amount of alcohol consumption up to adulthood, but also showed increased FFA oxidation in the livers. In addition, increased level of very low density lipoprotein and hypoglucagonemia were found. 40 micrograms/kg of glucagon which is known as an inhibitory factor of apoprotein production in the liver, was injected for 2 weeks into the rat tail vein and resulted in apparent fatty liver and hypolipoproteinemia. Norepinephrine injection (1 mg/kg) caused plasma glucagon to be depressed in the rat as compared with adult alcohol rats. Plasma cyclic AMP response to glucagon was also depressed in these rats. From these results, it is suggested that the deranged glucagon secretion from the pancreas and lowered glucagon-induced cyclic AMP response would relate to the abnormal lipoprotein metabolism in the rat.
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PMID:[Experimental studies on lipoprotein metabolism in rats reared with liquid alcohol diet from the fetal life]. 298 81

Sixteen mongrel dogs were depancreatized and controlled with intravenous hyperalimentation that included fat emulsion (Intralipid) for four weeks. Plasma lipids, fat tolerance test, PHLA, and presence of fatty liver were investigated. Dogs were divided into three groups (A, B, and C) for the purpose of studying the effect of fat emulsion. Groups A(n = 6) and B(n = 5) were given fat emulsion 1g/kg/day and 2g/kg/day respectively. Group C(n = 5) was not given fat emulsion. Group B had increased plasma total cholesterol and phospholipid. Group A had a slight increase of TG only. Group C had decreased plasma total cholesterol and phospholipid, and became hypoglycemic sometimes. The ability to clear fat emulsion expressed as (K2) decreased significantly after the 14th day in group B only. LPL, determined by the PHLA test in groups B and C only, did not change significantly. It seemed that fat emulsion was utilized in part as FFA and ketone bodies. Infusion of fat emulsion did not lead to fatty liver when insulin was administered continuously. For the depancreatized condition, it appeared that fat emulsion could be useful when blood sugar was controlled with insulin.
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PMID:[Effect of intravenous administration of fat emulsion to depancreatized dogs]. 314 8

Since many patients with cardiomyopathy have a history of chronic ethanolism often associated with malnutrition, we have evaluated left ventricular (LV) function in alcoholics with fatty liver, who had no clinical evidence of cardiac or nutritional disease. During an afterload test of LV function the pressor response to angiotensin evoked a threefold rise of enddiastolic pressure in the alcoholic group which was substantially greater than the 4 mm Hg rise in control subjects. The stroke volume and stroke work response in the noncardiac alcoholic was significantly less than in controls. Diminished LV function was corroborated in the noncardiac alcoholic at rest, using a contractility index. To evaluate the dose-response relationship of ethanol in the production of cardiac malfunction, two groups of noncardiac alcoholic subjects were studied acutely at low and moderate dose levels. After 6 oz, ventricular function, myocardial blood flow, and metabolism were not significantly affected. After 12 oz, there was a progressive rise of end-diastolic pressure and decrease of stroke output at a mean blood alcohol level of 150 mg/100 ml, reverting toward control by 4 hr. The coronary effluent transiently evidenced leakage of cell constituents, despite an increase of coronary blood flow, suggesting a direct but reversible cardiac injury. Myocardial extraction of triglyceride was enhanced, whereas FFA uptake was reduced. A possible role of myocardial triglyceride accumulation in heart muscle was considered in pathogenesis. Chronic ingestion of 16 oz of Scotch daily by an alcoholic subject while on a normal diet produced, after 12 wk, a progressive increase of heart rate and size, circulation time, and venous pressure, and a ventricular diastolic gallop. Normal values were restored within 7 wk after interrupting alcohol. These several studies suggest that the cumulative effects of repeated ingestion of ethanol in intoxicating doses can produce diminished LV function before clinical evidence of cardiac abnormality, or heart disease not necessarily related to malnutrition.
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PMID:Ventricular function in noncardiacs with alcoholic fatty liver: role of ethanol in the production of cardiomyopathy. 430 60

Treatment of rats with allylisopropylacetamide results in two related effects that occur sequentially. After one injection, serum FFA concentration increases and fatty liver develops without any decrease in lipoprotein synthesis. With repeated administration of the drug, fatty acid mobilization continues and acetate incorporation into lipids increases. However, fatty liver disappears with a concomitant increase in lipoprotein synthesis, resulting in hyperlipemia. It is postulated that accumulation of the liver lipid might be a regulating factor in the synthesis and transport of lipoproteins.
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PMID:Mechanism of fatty liver development and hyperlipemia in rats treated with allylisopropylacetamide. 554 7


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