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

Groups of normal and heterozygote sparse-fur (spf) mutant mice were studied at various stages of gestation, to assess the effects of normal pregnancy on orotate excretion, hepatic mitochondrial urea cycle enzymes and any predisposition to the development of fatty liver. Results show a higher total daily excretion of urinary orotate by normal pregnant mice on the 8th and 15th days of gestation, which came to within the usual basal range of excretion of non-pregnant mutant heterozygotes with hereditary ornithine transcarbamylase deficiency. Liver ornithine transcarbamylase and carbamyl phosphate synthetase-I activities were reduced in pregnant mice on the 16th day of gestation (P less than 0.05). No fatty change, bile stasis or glycogen depletion was discernible on optical microscopy in normal or mutant mice. Nonspecific changes were seen on ultrastructural examination. Orotic aciduria seen in pregnant mice may be directly related to a physiological deficiency of liver ornithine transcarbamylase. However, the depletion of both the mitochondrial urea cycle enzymes, seen on the 16th day of pregnancy, may be indicative of a metabolic stress at the mitochondrial level.
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PMID:The role of hepatic ornithine transcarbamylase deficiency in the orotic aciduria of pregnant mice. 373 88

This study provides confirmation of previous observations that showed that rats fed a diet containing 1% orotic acid for 7 days develop a fatty liver and that there is an inhibition of the secretion of low density lipoproteins without altering general liver protein synthesis. Accumulated fat droplets (liposomes) are entrapped within rough endoplasmic reticulum vesicles. In this study, these vesicles have been shown to accumulate the apolipoproteins of low and very low density lipoproteins. Inhibition of lipoprotein secretion was demonstrated by perfusion of livers from orotic acid-fed rats with a serum-free medium. Liposomes were isolated from these rats. Partially delipidated liposomes, but not similarly treated microsomes or cell sap, were found to form a precipitation line when reacted against anti-low density lipoprotein antiserum. Detergent solubilization of the liposome followed by density gradient centrifugation resulted in a peak at d 1.025 g/ml containing both lipid and protein. Acrylamide electrophoresis in 8 m urea after total delipidation demonstrated liposomal bands which coelectrophoresed with three of four very low density lipoprotein bands; there was no band corresponding to the very low density lipoprotein band which travels furthest in acrylamide electrophoregrams. However, acrylamide electrophoresis of the apoproteins of serum high density lipoprotein from orotic acid-fed animals revealed the presence of the latter band. The results indicate that liver liposomes from orotic acid-fed rats apparently contain the low density apoprotein and probably several other very low density lipoprotein peptides.
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PMID:Serum lipoprotein accumulation in the livers of orotic acid-fed rats. 436 41

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

Thirty-nine multiparous Holstein cows were used to measure the effect of propylene glycol treatment around parturition on milk yield, reproductive efficiency and some hormone and metabolite concentrations. Cows were assigned randomly to control (n = 19) or propylene glycol treated (n = 20) groups. Propylene glycol (300 g) was administered directly mixed with the diet from day 10 prior to the expected calving date until parturition (day 0) and orally after dilution in 1 l water on days 3, 6, 9 and 12. Blood samples were collected on days -20, -5, 0, 3, 10, 25 and 50 while milk samples were taken weekly until 13 weeks post partum. Body condition scores, recorded on days -20, 15 and 50, were not affected by propylene glycol administration. Propylene glycol did not significantly affect milk yield or composition but linear somatic cell score measured from the first 13 weeks post partum was reduced by propylene glycol administration (P < 0.01). Moreover, propylene glycol reduced milk urea (-25 mg/l, P < 0.05), especially during the first 9 weeks post partum. Plasma insulin concentrations were similar in both groups during the experiment while insulin-like growth factor I (P < 0.05) and insulin-like growth factor-binding protein 3 (P < 0.001) levels were higher on days 10, 25 and 50 post partum in the propylene glycol group. Propylene glycol administration decreased plasma non-esterified fatty acid concentrations (P < 0.05 to P < 0.01) but increased total cholesterol levels (P < 0.01) after parturition while 3-hydroxybutyrate levels were unaffected by the treatment. Changes in the hormone and metabolic concentrations after propylene glycol administration in the last few days of gestation and the first week of lactation seem to indicate that energy balance in the treated group was probably more positive than in the control group. There was also evidence that propylene glycol administration prevented fatty liver syndrome and hastened the resumption of oestrous cycles (P < 0.001).
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PMID:Effect of propylene glycol supplementation around parturition on milk yield, reproduction performance and some hormonal and metabolic characteristics in dairy cows. 865 35

We have analyzed diagnostic efficiencies of the individual "Essential laboratory test" items when these tests were applied to 520 new outpatients in the division of comprehensive medicine in a teaching hospital. The integration of these test results with history-taking and physical examination resulted in 544 primary clinical diagnoses which corresponded to the patient's illness complained and in 361 additional diagnoses unrelated to their chief complaints but found by chance by the addition of the test results. Clinical usefulness of these test items were variable depending on the disease category, demonstrating a superior diagnostic efficiency in infectious or inflammatory diseases, liver and biliary tract diseases, hematological disorders or metabolic diseases such as hyperlipidemia and diabetes mellitus, but a lesser degree of usefulness in gastro-intestinal or neurogenic diseases. Urine urobilinogen could not establish its clinical usefulness because of extremely low diagnostic sensitivity even in liver diseases. The leukocyte differential count provided confirmatory information for infectious or inflammatory diseases and was helpful for the estimation of the etiologic nature of infectious diseases. This study failed to terminate a controversy for the adoption of sialic acid instead of erythrocyte sedimentation rate (ESR) in the "Essential laboratory test" items, since the former test showed lower sensitivity, even though higher specificity, in infectious or inflammatory status than ESR. Low albumin globulin ratio (A/G) revealed equivalent diagnostic sensitivity and specificity to the elevated levels in alpha 1 and/or alpha 2 globulin fractions in infectious or inflammatory status, being helpful for the evaluation of patient's general condition at a glance. Incidental analysis for diagnostic values of cholinesterase and random blood glucose for the detection of fatty liver and diabetes mellitus, respectively, suggested that these two tests may be included in the "Essential laboratory tests". Simultaneous measurement of serum creatinine and blood urea nitrogen levels was recommended for the ambulatory screening of renal insufficiency, rather than the measurement either alone. The results in this study provide scientific bases on the usefulness of the individual test items and should be taken into account in the next version of the "Essential laboratory tests".
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PMID:The results of the "essential laboratory tests" applied to new outpatients--re-evaluation of diagnostic efficiencies of the test items. 875 34

Systemic carnitine-deficient juvenile visceral steatosis (JVS) mice exhibit decreased expression of some liver-selective genes including those for the urea cycle enzymes during the infantile period. At 25 days, carbamoylphosphate synthetase (CPS) mRNA level was remarkably low in the liver of JVS mice, and the HNF-4 and C/EBP-alpha mRNA contents were also reduced. HNF-3 alpha and C/EBP-beta mRNAs were slightly higher in the liver of JVS mice, and HNF-1 mRNA remained normal. These results, together with the developmental changes of these transcription factor mRNA levels, suggest that HNF-4 and C/EBP-alpha are involved in the suppression of CPS expression. If JVS mice survived the crisis at 4-5 weeks, their body weight caught up with that of control mice around 7 weeks. The steady-state levels of CPS and argininosuccinate synthetase (ASS) mRNAs in the liver of JVS mice were normalized by no later than 8 weeks. Starvation for 48 h caused an increase of about twofold in CPS and ASS mRNA levels in the liver of control mice, while the same treatment failed to increase their levels in the liver of JVS mice. The starvation similarly caused increases in HNF-4 and C/EBP-beta mRNA levels in the liver of both control and JVS mice, but the increases were significantly less in JVS mice than in control mice. Thus, the lack of induction of CPS and ASS mRNAs during development and under starvation in JVS mice correlated with the lower induction of HNF-4 and C/EBP-alpha mRNAs, and of HNF-4 and C/ EBP-beta mRNAs, respectively. Furthermore, all these changes seemed to correlate with the presence of fatty liver and the high serum free fatty acid levels, suggesting that disturbance of fatty acid metabolism affects nitrogen metabolism at least in part via altered gene expression of transcription factors such as HNF-4, C/EBP-alpha, and C/EBP-beta.
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PMID:Suppressed expression of the urea cycle enzyme genes in the liver of carnitine-deficient juvenile visceral steatosis (JVS) mice in infancy and during starvation in adulthood. 905 9

A Jersey herd was investigated following a decrease in milk yields. The cattle were permanently housed and fed a complete diet in four groups on the basis of yield. They were generally healthy, but the dry cows and many of the milking cows were over fat. The plasma concentrations of beta-hydroxybutyrate and glucose were normal, but the activities of aspartate aminotransferase and glutamate dehydrogenase and the concentration of non-esterified fatty acids were high. Fatty liver syndrome was diagnosed. All the dry cows were condition scored and placed into one of three dietary groups according to their score. They were exercised in an outdoor paddock and entered the pre-calving feeding group at least two weeks before calving; 75 per cent of them achieved a condition score of less than 3, and most of them produced normal milk yields. Thirty cows which had developed signs of fatty liver syndrome were paired and one of each pair received an injection of 640 mg of recombinant bovine somatotrophin. The yield of the treated cows was significantly higher (P < 0.05) for the first two weeks after the injection. The treated cows had higher plasma concentrations of beta-hydroxybutyrate and non-esterified fatty acids and lower plasma urea concentrations seven days after the injection. No other biochemical parameters were affected.
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PMID:Control of fatty liver syndrome in a Jersey herd by a change of diet and the use of recombinant bovine somatotrophin. 948 26

Two experiments were conducted to test the following two hypotheses: 1) fatty liver could hamper hepatic conversion of ammonia to urea and increase circulating ammonia or Gln% [Gln% = Gln x 100/(Gln + Glu)] in cows around parturition; 2) decreased ureagenesis might cause alkalosis and in turn reduce blood Ca. In the first experiment, 14 Holstein cows were monitored from 27 d prepartum to 35 d postpartum. There was a rise in circulating ammonia and Gln% at calving, suggesting an increase in ammonia passing to and through the liver. Stepwise regression analysis revealed the following relationship for plasma samples at 22 h and liver triglyceride at 2 d postpartum: ammonia (microM) = 32.1+/-0.89 triglyceride (% DM), Gln% = 71.2 + 0.23 triglyceride (% DM) + 1.31 urea (mM). The positive correlation between liver triglyceride and plasma ammonia and Gln% suggests that hepatic triglyceride accumulation might inhibit ureagenesis, thereby increasing ammonia concentration at the perivenous hepatocytes where Gln synthesis occurs and increasing ammonia concentration in blood leaving the liver. In the second experiment, 28 rats were used to determine whether hepatic triglyceride accumulation, induced by choline deficiency, affects urinary ammonia N and blood pH homeostasis. There was a trend for a positive correlation between urinary ammonia N and liver triglyceride. No correlation between liver triglyceride and blood pH, bicarbonate, pCO2 or plasma Ca was found. In conclusion, hepatic triglyceride accumulation may inhibit ureagenesis and result in increased circulating ammonia, Gln% and urinary ammonia N in vivo. Hepatic triglyceride accumulation did not affect blood pH homeostasis.
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PMID:Plasma concentration of urea, ammonia, glutamine around calving, and the relation of hepatic triglyceride, to plasma ammonia removal and blood acid-base balance. 1079 89

An increasing number of women with inborn errors of metabolism are now reaching child-bearing age. For certain disorders there are maternal risks associated with pregnancy. These may be related to an increased likelihood of metabolic decompensation (e.g. disorders of the urea cycle) or to increased stress to systems already compromised by disease (e.g. cardiomyopathy in GSD III). Detrimental effects upon the fetus may also be caused by maternal disease, as occurs with phenylketonuria, or from medication used to treat the mother's condition. Less commonly, fetal inborn errors may adversely effect the mother's health--e.g. fetal long-chain acyl-CoA dehydrogenase deficiency and the maternal HELLP syndrome (haemolysis, elevated liver enzymes and low platelets) and AFLP (acute fatty liver of pregnancy). Because of the rarity of individual disorders, our knowledge of risks associated with pregnancy is limited. Even for more common inborn errors such as phenylketonuria, there remain a number of questions that have not been fully answered.
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PMID:Inborn errors of metabolism and pregnancy. 1086 39

Type B lactic acidosis is a rare and often fatal complication seen in patients receiving the nucleotide analogues zidovudine, stavudine, didanosine, and lamivudine. We describe a case of a 51-year-old human immunodeficiency virus (HIV)-positive woman receiving three nucleotide analogues. She presented with nausea, vomiting, abdominal pain, and hepatic steatosis. Signs of mitochondrial toxicity were demonstrated by diffuse myopathy and pancreatitis. Serum riboflavin levels documented a deficiency that was treated with 50 mg of riboflavin daily. Immediately after treatment, serum blood urea nitrogen level, lactic acid levels, and arterial blood pH all returned to normal values. Her signs of mitochondrial toxicity also improved after treatment with riboflavin. Successful reversal of the patient's type B lactic acidosis after riboflavin therapy suggested that riboflavin deficiency plays a direct role in the development of nucleotide analogue-induced lactic acidosis. It is impossible to predict which patients are predisposed to the development of this syndrome. For this reason, it may be important to screen and treat riboflavin deficiency in patients on nucleoside analogues.
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PMID:Emerging role of riboflavin in the treatment of nucleoside analogue-induced type B lactic acidosis. 1178 75


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