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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 38-year-old female was admitted to our hospital because of dyspnea. The diagnosis of total lipodystrophy was made by following findings: (1) gaunt appearance; (2) insulin-resistant diabetes mellitus; (3) hyperlipidemia; (4) fatty liver. Chest X-ray demonstrated cardiomegaly, pulmonary edema and pleural effusion. Echocardiogram was characterized by left ventricular hypertrophy with asymmetrical septal hypertrophy and left ventricular dysfunction. Renal biopsy revealed focal glomerulosclerosis. We reported a patient with total lipodystrophy combined with heart failure and renal failure, which have been rarely associated with the disease.
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PMID:Total lipodystrophy with heart failure and renal failure: report of a case. 253 Mar 77

Techniques are reviewed for the experimental feeding of alcohol, including a liquid diet procedure invented 25 years ago. This technique results in much higher ethanol intake than with other approaches. As a consequence, various complications observed in alcoholics can be reproduced in animal models. These include fatty liver, hyperlipemia, various metabolic and endocrine disorders, tolerance to ethanol and other drugs, physical dependence and withdrawal and, in the baboon, liver fibrosis and cirrhosis. Variations of the liquid diet formulation are compared, and adequacy of nutrition in terms of minerals, vitamins, lipotropes, carbohydrates and proteins is discussed. The importance of selecting proper controls is emphasized. The respective advantages of three standardized basic rat formulas are reviewed: (i) an all-purpose (35% fat) diet, comparable to the diet previously referred to as the "Lieber-DeCarli formula" and suitable for most experimental applications, particularly those intended to mimic the clinical situation in which the various effects of alcohol occur in the setting of hepatic changes characterized by a fatty liver; (ii) a low-fat diet comparable in all respects to the preceding diet but with a lower fat content, intended to minimize the hepatic changes, and (iii) a high-protein formula particularly useful in those circumstances in which an oversupply of dietary protein might be recommended (i.e. pregnancy). Variations of this technique, including continuous intragastric infusion, are also discussed. It is concluded that, for most experimental studies of chronic alcohol consumption, the liquid diet technique provides one of the most efficient tools to study the effects of ethanol under controlled nutritional conditions because it allows for alcohol consumption of clinical relevance and offers flexibility to adjust to special experimental or physiologic needs by allowing for various substitutions required for a particular experimental design, including changes in lipids, proteins or other dietary constituents. The technique also facilitates the comparison with controls by simplifying the pair feeding and is the best procedure available for the study of the toxic effects of alcohol and their interactions with deficiency or excess of various nutrients.
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PMID:Experimental methods of ethanol administration. 267 71

In a cross-sectional health screening 636 persons with negative urine glucose, a 75-g-oral glucose tolerance test was performed. We report the clinical features of the subjects with impaired glucose tolerance or diabetes mellitus. In 96 subjects with impaired glucose tolerance, the frequencies of alcohol dependency, fatty liver, and of increased levels of serum uric acid, cholesterol, triglycerides, total serum protein and gamma-glutamyl transpeptidase were significantly higher than in normal subjects. In 37 subjects with diabetes mellitus, the frequencies of fatty liver, hypertension and of increased erythrocyte sedimentation rate, triglycerides and gamma-glutamyl transpeptidase were significantly higher than in normal subjects. In addition, significant increases in serum gamma-glutamyl transpeptidase, triglycerides, serum total cholesterol and body mass index, and a significant decrease in high density lipoprotein cholesterol were also observed in subjects with impaired glucose tolerance and diabetes mellitus. These results suggest that alcohol dependency, fatty liver, obesity and hyperlipidemia are important concomitants of impaired glucose tolerance.
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PMID:Study on background factors associated with impaired glucose tolerance and/or diabetes mellitus. 278 10

A high cholesterol/cholate diet induced hypercholesterolemia and fatty liver in both spontaneously hypertensive rats (SHR) and normotensive control rats (WKY). However, in contrast to previous concepts, the levels of cholesterol ester, triacylglycerol and phosphatidylcholine in plasma as well as triacylglycerol in liver were higher in WKY than in SHR fed a normal diet. The high cholesterol/cholate diet elevated the levels of plasma cholesterol, plasma cholesterol ester and hepatic triacylglycerol, and the extent of elevation was significantly higher in WKY than in SHR. Increases both in monoene/saturated ratios, an indication of elevated delta 9-desaturase activity, and in linoleate/arachidonate ratios, a possible indication of impaired desaturation-elongation activity, were observed in hepatic and plasma lipids of both strains fed the high cholesterol/cholate diet. The increases in monoene/saturated ratios were similar in both strains, but the increases in the linoleate/arachidonate ratios were higher for the plasma cholesterol esters of WKY than of SHR. The n-6/n-3 ratios of plasma and hepatic lipids were higher in WKY than in SHR throughout the experiments. These diet-induced changes observed in hepatic and plasma lipids were not reflected in the aortic lipids. Thus, hypertension per se does not promote the development of hyperlipemia and fatty liver induced by a high cholesterol/cholate diet. Our results also suggest that the metabolism of polyenoic fatty acids is different between SHR and WKY.
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PMID:Hypertension does not stimulate the development of hypercholesterolemia or fatty liver induced by a high cholesterol/cholate diet in rats. 280 64

A 36-year-old woman was treated with tamoxifen for lung metastasis of breast cancer and had marked hyperlipoproteinemia with giant fatty liver, high plasma triglyceride levels (3673 mg/dl), and increased levels of very low density lipoprotein (VLDL) and intermediate density lipoprotein (UDL). A low level of activity of both plasma lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) was also noted. Our observations support the concept that, in some patients, the weak estrogen-like activity of tamoxifen is amplified and, in severe lipemia, reduction of the activities of LPL and HTGL might impede the conversion of VLDL to LDL, thus causing the amplification of the effect.
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PMID:[A case report of hyperlipemia with giant fatty liver during adjuvant endocrine therapy by tamoxifen]. 310 57

To develop experimental fatty liver, Wistar male rats were fed a high fat, high cholesterol (Cho) diet for 6 weeks after which their diet was changed to standard chow. The animals were then divided by random selection into a sedentary group (SG) and four treadmill exercise groups for 6 weeks as follows: walking group (WG, 10 m/min, 60 min); low-speed running group (LRG, 20 m/min, 30 min); middle-speed running group (MRG, 30 m/min, 20 min) and high-speed running group (HRG, 40 m/min, 15 min). The serum concentration of very low density lipoprotein (VLDL) and low density lipoprotein (LDL)-Cho decreased, and high density lipoprotein (HDL)-Cho increased in WG compared with the other three exercise groups. Hepatic triglyceride (TG) was significantly lower (P less than 0.05) in WG than in SG. Hepatic Cho was lower in HRG than in the other three exercise groups, and Cho in the aortic wall was higher. The results suggest that light exercise, such as walking might be more beneficial to lipid-lipoprotein metabolism than strong exercise, such as high-speed running. This is consistent with suggestion that light exercise might be effective in clinical treatment for hyperlipidemia, arteriosclerosis or fatty liver.
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PMID:Dependence of lipid-lipoprotein metabolism on exercise intensity in experimental fatty liver rats. 325 7

The effects of cotreatment with a hyperlipidemic chemical, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), and a hypolipidemic agent, di(2-ethylhexyl)-phthalate (DEHP), on lipid metabolism and toxicologic responses were studied in F344 rats. Treatment with TCDD alone (160 micrograms/kg) caused an increase in serum triglycerides and cholesterol while treatment with DEHP alone (2 g/kg/day) caused a decrease in triglycerides and cholesterol versus untreated controls. When administered before or after TCDD, DEHP caused a decrease in TCDD-induced hyperlipidemia. This change was attributed to enhanced hepatic peroxisomal beta-oxidation and decreased hepatic lipid synthesis resulting from treatment with DEHP. TCDD treatment produced a fatty liver, as determined by gravimetric analysis of extracted lipid and microscopic examination of liver sections which revealed extensive cytoplasmic vacuolization that stained positive with Oil Red 0, but did not induce peroxisomal beta-oxidation. Thus, an increase in hepatic or serum lipid levels is not sufficient for induction of peroxisome proliferation. Neither TCDD nor DEHP treatment affected mitochondrial beta-oxidation. Pretreatment of rats with DEHP, followed by daily exposure to this hypolipidemic agent after treatment with TCDD, had a partial protective effect against TCDD-induced fatty liver, body weight loss and mortality. Microscopic examination of liver sections confirmed the suppression of TCDD-induced fatty liver by pretreatment with DEHP. When DEHP treatment was initiated after the TCDD dose, there was less protection against the above parameters of TCDD toxicity. This study demonstrates that TCDD-induced fatty liver, hyperlipidemia and mortality can be antagonized by treatment with a hypolipidemic agent such as DEHP.
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PMID:Modulation of 2,3,7,8-tetrachlorodibenzo-p-dioxin toxicity in F344 rats by di(2-ethylhexyl)phthalate. 337 78

99mTc-diethyl-acetanilide-iminodiacetic acid (IDA) was compared with indocyanine green (ICG) as an indicator of hepatic blood flow (HBF). Twelve subjects (8 with cirrhosis, 2 with fatty liver, one with pancreatitis, and one with intestinal angina) were studied during hepatic vein catheterization. In 9 subjects the HBF measurements (indirect Fick-principle) were within 0.8-1.9 l/min, and no significant difference was observed between the values obtained by ICG and 99mTc-diethyl-IDA (mean 1.24 vs 1.26 l/min, P greater than 0.4). In 2 subjects with cirrhosis very high but almost identical values were found with the two indicators. In one subject ICG could not be measured in plasma because of hyperlipidaemia, but HBF was easily determined by 99mTc-diethyl-IDA. The results indicate that 99mTc-diethyl-IDA can be used as an indicator of HBF. This indicator is not superior to ICG in patients with decreased liver function, but offers advantages in that it can be used with small plasma samples and permits the determination of HBF in the presence of hyperlipidaemia.
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PMID:Hepatic blood flow determination. A comparison of 99mTc-diethyl-IDA and indocyanine green as hepatic blood flow indicators in man. 357 34

Sodium nitrite administered in the drinking water to Long-Evans rats during pregnancy and lactation severely affected erythropoietic development, growth, and mortality in their offspring. Pregnant rats were maintained throughout gestation on 0.5, 1, 2, or 3 g NaNO2/liter. There were no significant differences between treated and control litters at birth. Thereafter, pups of treated dams on 2 and 3 g NaNO2/liter gained less weight, progressively became severely anemic, and began to die by the third week postpartum. By the second week postpartum, hemoglobin levels, RBC counts, and mean corpuscular volumes of these pups were all drastically reduced compared to controls. Blood smears showed marked anisocytosis and hypochromasia. Gross chylous serum lipemia and fatty liver degeneration were noted. Histopathology demonstrated cytoplasmic vacuolization of centrilobular hepatocytes and decreased hematopoiesis in bone marrow and spleen. Administration of 1 g NaNO2/liter resulted in hematological effects but did not affect growth or mortality. NaNO2 (0.5 g/liter) was at or near the no observed effect level. Cross-fostering indicated that treatment during the lactational period was more instrumental in producing lesions than treatment during the gestational period. The data presented are consistent with the lactational induction of severe iron deficiency in the neonate.
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PMID:Evaluation of the developmental toxicity of sodium nitrite in Long-Evans rats. 369 23

Weanling male Hartley guinea pigs were fed for 6 weeks on a regular chow supplemented with 5% polyunsaturated fats (safflower, linseed, or evening primrose oil) or 5% saturated fats (hydrogenated coconut oil) with or without the addition of 1% cholesterol to the diet. Cholesterol feeding resulted in slower growth, hyperlipidemia, and a fatty liver. Cholesterol contents (predominantly in the form of cholesterol esters) in plasma and liver were increased, but the increase of plasma cholesterol was significantly reduced when unsaturated fats in place of saturated fat were added to the diet. The essential fatty acid contents in plasma and liver lipids were modulated by the dietary fats and by the cholesterol feeding. The latter reduced the proportions of 20:4 (n-6), but increased or had no effect on the levels of 18:2 (n-6). These results led to a reduced ratio of 20:4 (n-6)/18:2 (n-6), suggesting that cholesterol feeding may impair the desaturase activities.
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PMID:Effect of dietary cholesterol and polyunsaturated fats on plasma and liver lipids in guinea pigs. 382 3


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