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

A 54-year-old woman with obesity, type II diabetes mellitus, hyperlipidemia, and massive hepatomegaly was found to have severe steatosis and cirrhosis on liver biopsy. Complete evaluation led to the diagnosis of fatty cirrhosis associated with obesity and diabetic mellitus. She underwent four months of fasting with a protein-carbohydrate and vitamin-mineral liquid supplement to control her weight and metabolic abnormalities and to evaluate the effect of this diet on her liver disease. She lost 40 pounds to ideal body weight, normalized her serum glucose and lipids, and decreased total liver height by one third. Liver biopsy at the completion of her diet showed inactive cirrhosis and complete resolution of steatosis. Supplemented fasting with only modest weight loss can safely resolve fatty liver in obese diabetics with nonalcoholic steatosis and cirrhosis. Aggressive dietary approaches to achieve long-term weight loss deserve study in this subgroup of diabetics with unexplained chronic liver disease.
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PMID:Steatosis and cirrhosis in an obese diabetic. Resolution of fatty liver by fasting. 382 84

A high dose of methylprednisolone was administered intramuscularly to rabbits, and we studied the accumulation of lipid in the osteocytes of the femoral head by histochemical methods and electron microscopy. Advanced hyperlipidemia and a fatty liver were observed in four weeks. Electron microscopy was used to define the ultrastructural changes in osteocytes, which showed small lipid droplets that gradually enlarged, finally resulting in the formation of vacuolated vesicles. An increase in the size of the lipid droplets caused them to compress the nucleus to one side of the lacuna, resulting in discontinuities of the cell membrane followed by cell disintegration. These observations demonstrate the effect on osteocytes of a disturbance in lipid metabolism caused by the administration of large doses of steroids.
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PMID:Steroid-induced accumulation of lipid in the osteocytes of the rabbit femoral head. A histochemical and electron microscopic study. 399 28

The effect of nicardipine on experimental hyperlipemia induced by a 1% cholesterol diet in spontaneously hypertensive rats (SHR) was investigated by the change of hemodynamics and the determination of lipid contents of the serum, liver, heart and aorta. Nicardipine increased liver weight and liver weight per body weight ratio, and it decreased heart and kidney weight significantly. Nicardipine inhibited the increase in blood pressure with cholesterol and normal diets. Nicardipine decreased heart rate in SHR fed the normal diet, and it inhibited the increase in heart rate in SHR fed the cholesterol diet. Serum lipid levels significantly increased with the cholesterol diet. Nicardipine significantly increased cholesterol in high density lipoprotein (HDL-C) and phospholipid in HDL (HDL-PL) with cholesterol and normal diets, and it decreased triglyceride and improved the atherogenic index "(total cholesterol-HDL-C)/HDL-C" with the normal diet. Serum GOT and GPT significantly increased with the cholesterol diet. Nicardipine significantly enhanced an increase in GOT and GPT levels with the cholesterol diet. Nicardipine increased phospholipid content in the liver, triglyceride in the heart, and it decreased total cholesterol in the aorta. A morphologic study showed a fatty liver in SHR fed the cholesterol diet, but nicardipine had no effect on the morphological changes in the liver, heart and aorta. These results suggest that nicardipine may prevent atherosclerotic degeneration by the inhibition of hypertension, increase in serum HDL and decrease in total cholesterol in the aorta.
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PMID:[Effect of nicardipine on cholesterol-fed S.H.R]. 405 35

During its prolonged period of gestation, the fetal guinea pig gradually develops a striking hyperlipemia (plasma triglycerides ca. 500-1500 mg/dl) and fatty liver (hepatic triglycerides ca. 25% of wet weight). The parenchymal cells of the liver contain not only many fat droplets in the cytoplasm, but also large numbers of osmiophilic particles, interpreted as precursors of plasma lipoproteins, within profiles of the cisternae and secretory vesicles of the Golgi apparatus. Similar particles are found in intercellular spaces, in the space of Disse, and in the hepatic sinusoids. Near the end of gestation, these particles enlarge to the size range characteristic of chylomicrons secreted from the intestinal mucosa after ingestion of fat. At the same time, the hyperlipemia increases and is characterized by the accumulation of particles resembling chylomicrons morphologically and chemically. The results are interpreted as evidence of intense hepatic synthesis and secretion of very low density lipoproteins which may be related to the extensive transplacental transport of free fatty acids known to occur in this species. After birth, the hyperlipemia subsides rapidly and the hepatic steatosis more gradually. The blood plasma of the guinea pig fetus also contains moderate amounts of low density and high density lipoproteins. The latter decrease to barely detectable levels during the first 2 wk of postnatal life. Comparably low levels of high density lipoproteins are found in nonpregnant and pregnant adults.
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PMID:Physiological fatty liver and hyperlipemia in the fetal guinea pig: chemical and ultrastructural characterization. 433 57

Alcohol addicts with a primary type IV hyperlipoproteinemia show a striking elevation of triglycerides in the serum during long periods of alcohol consumption as compared with controls, without an accompanying significant increase in free fatty acids in the serum. These data suggest that this genetically related lipid abnormality may be a significant factor in the pathogenesis of alcohol hyperlipemia and the alcohol-induced fatty liver.
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PMID:Alcohol-induced hyperlipidemia and beta lipoproteins. 470 74

In vivo ethanol given acutely or chronically by two dietary means resulted in significant increases in [1-(14)C]palmitate incorporation into triglyceride by intestinal slices or microsomes derived from intestinal slices. In vitro, 2.6 percent ethanol, an amount comparable to that found in t..e intestinal lumen of social drinkers, also resulted in significant increases in [1-(14)C]palmitate incorporation into triglyceride. Pyrazole, an inhibitor of alcohol dehydrogenase, diminished the stimulatory effect of ethanol both in vivo and in vitro. These data may provide a new insight into the effects of alcohol, and specifically on the possible contribution of intestinal triglyceride synthesis to alcoholic hyperlipemia and the alcohol-induced fatty liver.
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PMID:Ethanol stimulates triglyceride synthesis by the intestine. 513 47

In rats, chronic ethanol feeding was found to enhance the postprandial hyperlipemia and to increase the incorporation of dietary palmitic acid-(3)H and intravenously injected L-lysine-(14)C into serum lipoproteins. The main increases of total amount, labeling, and specific activity of lipid and protein occurred in the d < 1.019 lipoprotein fraction. Fat absorption and the clearance of injected chylomicrons were not affected by ethanol feeding. Blocking of lipoprotein and chylomicron removal with Triton did not prevent the action of ethanol on serum lipids, indicating that the ethanol effect is not likely due to defective removal of lipids from the circulation. Ethanol enhanced the incorporation of chylomicron fatty acids into newly synthetized very low density lipoproteins, as shown by an increased reappearance of the fatty acid label into the lipids of this fraction after injection of palmitate-(14)C/glycerol-(3)H doubly labeled chylomicrons. These results indicate that alcoholic hyperlipemia is due, at least in part, to an increase in newly synthetized lipoproteins. The hyperlipemia produced by ethanol was accompanied by hepatic steatosis. The simultaneous production of fatty liver and hyperlipemia makes it unlikely that defective lipoprotein synthesis or secretion is a primary mechanism for the pathogenesis of the alcoholic fatty liver.
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PMID:Efcts of chronic ethanol feeding on serum lipoprotein metabolism in the rat. 544 77

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

Infection of 10-day-old chicken embryos with an avian retrovirus. Rous-associated virus type 7, resulted in a disease characterized by stunting and hyperlipidemia. By 20 days after hatch, infected chickens were smaller than hatchmates and developed ataxia and obesity over the next 30 days. Histological examinations of livers from infected chickens revealed a diffuse panlobular fatty infiltrate involving an accumulation of fat in microdroplets. Electron microscopic examinations of livers from infected chickens revealed hepatocytes with swollen mitochondria that lacked cristae. The thyroid and pancreas were infiltrated with lymphoblastoid cells by 1 week after hatch. An examination of the blood revealed a mild anemia, a frank lipemia, and high levels of uric acid. This syndrome induced by Rous-associated virus type 7 in chickens may be useful for elucidating the nature of several diseases, including that found in the fatty liver and kidney syndrome of chickens and that observed in a strain of obese chickens.
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PMID:Rous-associated virus type 7 induces a syndrome in chickens characterized by stunting and obesity. 629 59

The interaction of ethanol with lipid metabolism is complex. When ethanol is present, it becomes a preferred fuel for the liver and displaces fat as a source of energy. This favors fat accumulation. In addition, the altered redox state secondary to the oxidation of ethanol promotes lipogenesis, for instance, through enhanced formation of acylglycerols. The depressed oxidative capacity of the mitochondria injured by chronic alcohol feeding also contributes to the development of the fatty liver. Accumulation of fat acts as a stimulus for the secretion of lipoproteins and the development of hyperlipemia. Hyperlipemia may also be facilitated by the proliferation of the endoplasmic reticulum after chronic ethanol consumption and the associated increase of enzymes involved in the production of triglycerides and lipoproteins. The propensity to enhance lipoprotein secretion is offset, at least in part, by a decrease in microtubules and an impairment of the secretory capacity of the liver. The level of blood lipids depends on the balance between these two opposite changes: At the early stage of alcohol abuse, when liver damage is still small, hyperlipemia will prevail, whereas the opposite occurs with severe liver injury. When hyperlipemia occurs, it involves all lipoprotein classes, including high density lipoprotein (HDL). The latter have been suggested to be responsible for the lower incidence of coronary complications of moderate drinkers compared to teetotalers, but in fact, the subtype of HDL involved (HDL3) differs from the HDL2 subtype associated with protection.
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PMID:Ethanol and lipids. 638 65


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