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

The present study was aimed at demonstrating the effects of exercising in water at two different temperatures on lipid-lipoprotein metabolism in experimental fatty liver rats. The rats were fed a high fat, high cholesterol (CHL) diet for 6 weeks, then returned to standard chow. The fatty liver rats were then divided at random into three groups, two for swimming in 20 degrees C (20SWG) and 30 degrees C (30SWG) water, 5 days/week, 30 min/day for 6 weeks, and a sedentary control group (SG). The concentrations of serum triglyceride (TG) and CHL were significantly lower (p less than 0.01) in both the 20SWG and 30SWG than in the SG. The serum concentration of very low density lipoprotein (VLDL)-CHL was clearly less in the 20SWG than in the SG (p less than 0.05) or the 30SWG (p less than 0.01). Compared to the SG, the two swimming groups had significantly lower levels (p less than 0.01) of low density lipoprotein (LDL)-CHL. The LDL-CHL in the 30SWG was significantly lower (p less than 0.01) than that in the 20SWG. There were no significant differences among the three groups in high density lipoprotein (HDL)/CHL. However, the ratio of HDL to CHL was over 10% greater in the two swimming groups than in the SG. Hepatic CHL ester and TG were significantly lower (p less than 0.05) in the 20SWG than in the SG. These results indicate that swimming in water at the lower temperature was more stimulating to lipid-lipoprotein metabolism in fatty liver than swimming in the higher temperature water.
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PMID:Effects of swimming exercise at two different water temperature on hepatic lipid and lipoprotein levels in experimental fatty liver rats. 263 61

The supply of ethanol and other substances to the rat has necessitated the development of quite complex dietary preparation and feeding techniques. This study reports the use of ethanol/water solutions in conjunction with normal rat chow diet to provide up to 30 g/kg/day ethanol to study animals. By additionally supplying agar gels containing ethanol, voluntary intake of ethanol was raised to a possible maximum of 48 g/kg/day. Hepatic steatosis was produced in 7/18 rats supplied ethanol in this fashion. Agar gels were also used to provide carbonyl iron to rats and it produced grade 3 to 4 hepatocyte iron loading in all study animals. The study demonstrates a practical method for administering ethanol and iron to rats without altering normal dietary intake. Ethanol supplied in this way does produce hepatic injury in the rat.
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PMID:A histological study of the use of agar as a delivery vehicle for alcohol or iron to rats. 271 91

Chemical shift is the phenomenon that is seen when an isotope possessing a nuclear magnetic dipole moment resonates at a spectrum of resonance frequencies in a given magnetic field. These resonance frequencies, or chemical shifts, depend on the chemical environments of particular nuclei. Mapping the spatial distribution of nuclei associated with a particular chemical shift (e.g., hydrogen nuclei associated with water molecules or with lipid groups) is called chemical shift imaging. Several techniques of proton chemical shift imaging that have been applied in vivo are presented, and their clinical findings are reported and summarized. Acquiring high-resolution spectra for large numbers of volume elements in two or three dimensions may be prohibitive because of time constraints, but other methods of imaging lipid of water distributions (i.e., selective excitation, selective saturation, or variations in conventional magnetic resonance imaging pulse sequences) can provide chemical shift information. These techniques require less time, but they lack spectral information. Since fat deposition seen by chemical shift imaging may not be demonstrated by conventional magnetic resonance imaging, certain applications of chemical shift imaging, such as in the determination of fatty liver disease, have greater diagnostic utility than conventional magnetic resonance imaging. Furthermore, edge artifacts caused by chemical shift effects can be eliminated by certain selective methods of data acquisition employed in chemical shift imaging.
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PMID:Chemical shift imaging: a review. 300 43

Sixteen patients given total pancreatectomy were experienced, and the essential points of postoperative management were reported. The morbid states after total pancreatectomy consist of: a deficiency of pancreatic endocrine function, a deficiency of pancreatic exocrine function, loss of the duodenum and upper jejunum, the influence of partial or total gastrectomy, and the influence of dissection around the superior mesenteric artery. These states influence each other and become more complicated. The management period is divided into five parts as follows; a period of intravenous nutrition, the early half; water replacement period, the late half; hyperalimentation period, a period of intravenous and enteral nutrition, a period of enteral, intravenous and oral nutrition, a period of oral and enteral nutrition, and a period of oral nutrition. In each period, a special form of management is needed. The essential points of long-term management are as follows: The use of suitable doses of pancreatic enzyme and antidiarrheal agents for the cure of severe maldigestion and malabsorption. Also, intermittent IVH or elemental diet are effective for recovery from deteriorative malnutrition. For the prevention of hypoglycemic attack, training of the patients and the maintainance of good nutrition are important. These patients have a high incidence of infection, and so speedy treatment must be given if this occurs. Fatty liver must be treated by intermittent IVH or elemental diet. As total pancreatectomy imposes a severe burden on the patient, including self-injection of insulin, the indications of this operation must be decided carefully giving due consideration to its radicality.
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PMID:[Postoperative management of total pancreatectomy]. 309 14

Although young infants are at greater risk for total parenteral nutrition (TPN)-related liver disease than adults, previous studies on the effect of the TPN energy source on the development of hepatic steatosis have been carried out in adult rats and adult humans. We studied the effect of a glucose and a glucose/fat TPN energy regimen on hepatic chemical composition and the development of steatosis in newborn miniature pigs. Twenty miniature pigs were randomized at 10 days of age to receive a TPN regimen which utilized either glucose (group A) or glucose/fat (group B) as the non-nitrogen energy source. After 8 days, blood was drawn for insulin, glucagon, SGPT, albumin, and bilirubin determinations. Samples of liver were obtained at 9 days. Plasma insulin levels were significantly higher and glucagon levels lower in group A piglets than in those in group B. Normal values were obtained for SGPT, albumin, and bilirubin, and no differences were found between groups. Chemical analysis of the livers revealed no differences between groups in the concentrations of glycogen, fat, protein, DNA, and RNA. Group A animals had significantly higher concentrations of water than group B (group A: 0.75 +/- 0.01 liter/kg; group B: 0.74 +/- 0.01; p less than 0.03). A significant correlation was found in group B between the plasma insulin/glucagon ratio and the hepatic glycogen concentration (r = 0.73, p less than 0.05). Group A animals had fat vacuoles in centrilobular hepatocytes, in contrast with group B animals who had visible fat only in Kupffer cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Liver composition and histology in growing infant miniature pigs given different total parenteral nutrition fuel mixes. 311 Apr 45

A 22-year old woman in the 37th week of her third pregnancy (twins) developed acute fatty liver complicated with a haemorrhagic syndrome from disseminated intravascular coagulation. Two normal girls were delivered by caesarean section. Persistent surgical bleeding required hysterectomy and a short stay in an intensive care unit. The disseminated intravascular coagulation subsided within 8 days. Three weeks after delivery a pituitary insufficiency (Sheehan's syndrome) was diagnosed. A second liver biopsy showed that the lesions had regressed. One week after delivery, the patient developed polyuria and polydipsia. The diagnosis of diabetes insipidus was confirmed by the lack of increase of plasma antidiuretic hormone level during an 8-hour water deprivation test. The pathophysiology of these different syndromes is discussed. Disseminated intravascular coagulation might be the link between hypopituitarism and diabetes insipidus.
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PMID:[Twin pregnancy with acute hepatic steatosis followed by antehypophyseal insufficiency and diabetes insipidus]. 316 Oct 48

Chronic ethanol consumption results in the induction of a specific hepatic cytochrome P-450 (P450IIE1). However, since compounds other than ethanol (i.e., acetone) can also serve as P450IIE1 inducers, and since ethanol given with a normal fat-containing (35% of energy) diet is associated with acetonemia, hepatic steatosis and decreased body weight gain, the question has been raised whether induction is mediated specifically by ethanol or whether it might represent a nonspecific response to these other factors. This was investigated by varying both the mode of ethanol administration and the composition of the diet. By administering ethanol in the drinking water, or as part of a low-fat (5% of energy) liquid diet, a significant induction of P450IIE1 and of the activities of the microsomal ethanol oxidizing system and p-nitrophenol hydroxylase was demonstrated in the absence of any significant increase in blood acetone with minimal increase in liver total lipids. Induction of P450IIE1 was comparable with the low or normal fat-containing diets, but MEOS activity rose more with the latter, possibly reflecting a potentiating effect of dietary fat on ethanol oxidation by P-450 enzymes other than P450IIE1. When the lack of weight gain of the alcohol fed animals was mimicked in controls by decreasing the amount of diet ingested, no induction was observed. Varying the pattern of liquid diet feeding had no demonstrable differential effect. Thus, the induction of P450IIE1 after chronic ethanol consumption can be attributed to ethanol itself, but dietary fat can potentiate the induction of the microsomal ethanol oxidizing system and of p-nitrophenol hydroxylase.
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PMID:Role of acetone, dietary fat and total energy intake in induction of hepatic microsomal ethanol oxidizing system. 318 73

Neonatal rats from dams receiving 2 or 3 g NaNO2/liter in the drinking water through -gestation and lactation suffered severe microcytic anemia as well as growth retardation and high mortality. Lipemia, fatty liver damage, decreased erythropoiesis of spleen and bone marrow, and reduced plasma and tissue iron levels were noted in affected pups. These effects were all consistent with and characteristic of iron deficiency. Experiments presented here were designed to show that the maternally mediated toxicity of nitrite is actually an iron deficiency syndrome in the pups caused by inadequate iron transfer from dam to pup. It was found that administration of exogenous iron supplement to pups of treated mothers reversed the anemia and other effects of nitrite toxicity noted both in previous studies and in unsupplemented littermates. Mothers of affected pups were themselves anemic. Finally, we fully documented severe iron deficiency in pups of nitrite-treated mothers and showed that these mothers produced milk of reduced iron content. It appears then that nitrite-consuming dams have a reduced capacity to transfer iron to their pups. The nitrite-associated toxicities in the pups are actually a result of an iron deficiency.
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PMID:Nitrite-induced iron deficiency in the neonatal rat. 318 25

The effects on the ultrasonic propagation properties of livers of the addition of 1% orotic acid to rat diets were examined. In rats, dietary orotic acid exerts several effects on lipid metabolism; its overall consequence is that excessively high hepatic fat concentrations are built up over a short period of time, thus making this an ideal model to study the ultrasonic propagation properties as a function of sequential development of fatty liver. Over a 16-day period on the orotic acid diet, the supplemented rat liver lipid concentrations increased from a normal range of 2%-4% to the lower 20's%; hepatic water concentration decreased from a normal value of approximately 70% to approximately 50%; total protein concentration decreased slightly from a normal range of 17%-20% to 11%-16%; and rat liver weight increased from approximately 11 g to around 20 g. Ultrasonic attenuation coefficient and speed were assessed in liver tissue with the scanning laser acoustic microscope at 100 MHz. As hepatic lipid increased, ultrasonic attenuation at 100 MHz increased temporally from a normal range of 12-14 dB/mm to a maximum of 54 dB/mm and ultrasonic speed decreased from a normal range of 1553-1584 m/s to a minimum of 1507 m/s. Multivariant linear regression was used in the analysis of covariance to fit the least-squares estimates to the linear regression model. Strong correlates of ultrasonic speed with both water concentration and fat concentration in the liver were observed.
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PMID:Ultrasonic propagation properties (@ 100 MHz) in excessively fatty rat liver. 328 85

To accelerate the synthesis of endogenous lipids, Wistar male rats were administered sucrose solution and standard chow diet for 5 weeks. The diet was then changed to tap water plus a high-cholesterol (Cho) diet and the animals were subjected to treadmill running for 5 weeks. The concentrations of serum triglyceride (TG) and very low density lipoprotein (VLDL)-cho in the group that had endurance exercise and was fed high-Cho diet were significantly lower than those in the non-exercise group that was fed high-Cho diet. However, the exercise-high-Cho group accumulated quantities of lipids in the liver similar to the non-exercise-high-Cho group and developed a markedly fatty liver. In conclusion, it is suggested that long-term exercise did not accelerate hepatic lipid metabolism and seemed to suppress synthesis and release of VLDL in the liver.
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PMID:Effects of long-term exercise and high-cholesterol diet on lipid-lipoprotein metabolism in rats. 350 94


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