Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The lipid-lowering effect of carnitine and its precursors, namely lysine plus methionine, was examined in male Sprague-Dawley rats fed ethanol as 36% of the total calories. Ethanol caused typical hepatic steatosis characterized by significant accumulation of total lipids, triglycerides, cholesterols, phospholipids, and free fatty acids. Supplementation of the ethanol diet with 1% DL-carnitine, 0.5% L-lysine, and 0.2% L-methionine significantly lowered ethanol-induced increases of various lipid fractions, with the exception of free fatty acids. The lipid-lowering effect of carnitine was superior to that of its precursors and their effect together was no greater than that of carnitine alone. The triglyceride contents of liver and plasma were related inversely to the levels of carnitine and acyl carnitines. It is concluded that dietary carnitine more effectively than its precursors prevented alcohol-induced hyperlipemia and accumulation of fat in livers. Thus, a deficiency of functional carnitine may indeed exist in chronic alcoholic cases.
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PMID:Ameliorating effects of carnitine and its precursors on alcohol-induced fatty liver. 642 29

To study the effects of alcoholic liver injury on the ability of ethanol to promote hepatic fat accumulation and hyperlipemia, baboons were pair-fed liquid diets containing 50% of energy either as ethanol or as additional carbohydrate (controls) for 1 to 7 years. Alcohol consumption produced triacylglycerol accumulation in the liver, hypertriacylglyceridemia, and various degrees of liver injury, including cirrhosis. At the early stages of fatty liver (with or without perivenular fibrosis), there was increased activity of microsomal diacylglycerol acyltransferase and of both microsomal and cytosolic phosphatidate phosphohydrolase, with no changes in glycerol-3-phosphate acyltransferase. With progression of the liver injury and development of septal fibrosis and/or cirrhosis, the rate of hepatic triacylglycerol accumulation and the magnitude of the hyperlipemia decreased, despite continuous ethanol intake. These changes were associated with disappearance of the increases in microsomal diacylglycerol acyltransferase and cytosolic phosphatidate phosphohydrolase activities, whereas those of microsomal phosphatidate phosphohydrolase remained elevated and glycerol-3-phosphate acyltransferase was unaffected. Thus, changes in the activity of two enzymes of the triacylglycerol-synthesizing pathway, namely the microsomal diacylglycerol acyltransferase and the cytosolic phosphatidate phosphohydrolase, may contribute to the differences in the rate of hepatic triacylglycerol accumulation and the degree of hyperlipemia during progression of the alcoholic liver damage.
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PMID:Hepatic triacylglycerol synthesizing activity during progression of alcoholic liver injury in the baboon. 649 27

A 40-year-old man was diagnosed as fatty liver according to our ultrasonographical criteria for fatty liver, i.e., liver-kidney contrast in the ultrasound mass screening of the liver, biliary tract and pancreas. He lacked any signs or symptoms, nor any known causes of fatty liver, i.e., obesity, diabetes, hyperlipidemia, ingestion of alcohol or drugs. Liver biopsy of this patient revealed fatty change of about 50% of the hepatic lobules. It has been difficult to suspect the presence of latent fatty liver which lacked both the abnormality in the liver function test and hepatomegaly, and even impossible when it lacked any risk factors. In the future as the ultrasonography becomes more generally used as a primary screening examination, "idiopathic latent fatty liver", like this patient, will be more frequently found and this, in turn, will contribute to the progress of the epidemiology and etiology of fatty liver.
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PMID:A case of idiopathic fatty liver detectable only by ultrasonography. 662 57

Effects of Panax ginseng on plasma and hepatic lipids were investigated in the high cholesterol diet-fed rats and in patients with hyperlipidemia. Oral administration of red ginseng powder reduced plasma total cholesterol, triglyceride and NEFA, while plasma HDL-cholesterol was elevated. Platelet adhesiveness was also reduced by ginseng administration. The plasma lipid-improving actions were also observed in patients with hyperlipidemia. Hepatic cholesterol and triglyceride contents were decreased and phospholipid increased by ginseng administration in the high cholesterol diet-fed rats, corresponding to improvement of the fatty liver.
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PMID:Serum HDL-cholesterol-increasing and fatty liver-improving actions of Panax ginseng in high cholesterol diet-fed rats with clinical effect on hyperlipidemia in man. 666 Feb 21

A sub-strain of male and female spontaneously hypertensive rats (SHR) capable of having massively obese or non-obese offspring were bred repeatedly or were maintained as virgin controls. When the male and female breeders had sired or given birth to 5 litters of young, they were autopsied along with their 10-month-old celibate brothers and sisters. Virgin and breeder SHR developed high blood pressure (250 +/- 10 mm Hg). Breeder rats were significantly heavier than their virgin cohorts; pituitary and adrenal glands, hearts, and kidneys were significantly enlarged while thymi were severely involuted in breeder vs virgin SHR. The hyperlipidemia, fatty liver, hyperglycemia, and islet hyperplasia, characteristic of virgin SHR, were greatly exacerbated in breeder SHR. Blood levels of corticosterone, deoxycorticosterone, and aldosterone were greatly elevated in breeder vs virgin SHR. Although breeder rats of genetically normotensive strains develop aortic sclerosis, none of the breeder SHR developed aortic sclerosis. Instead, intimal fibrinohyalin lesions appeared confined to the testes and ovaries. It is suggested that the anatomical appearance or resistance of the arterial wall to the development of lesions is genetically mediated but this genetic programming may be modified by metabolic and hormonal factors with particular emphasis on the participation of adrenocorticoids.
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PMID:Hyperlipidemia, hyperglycemia and hypertension in repeatedly bred parents of the obese spontaneously hypertensive rat (obese/SHR) unaccompanied by arteriosclerosis. 674 80

The technique of feeding ethanol as part of a totally liquid diet was invented two decades ago and its successful application for the intervening period is reviewed. This technique results in much higher ethanol intake than with conventional procedures. As a consequence, various complications observed in alcoholics were reproduced in animal models, including fatty liver, hyperlipemia, various metabolic and endocrine disorders, tolerance to ethanol and other drugs, physical dependence and withdrawal, the fetal alcohol syndrome and, in the baboon, liver fibrosis and cirrhosis. Variations of the liquid diet formulation are compared and three standardized basic formulas are being proposed for the rat: (1) a regular 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 liver changes characterized by a fatty liver; (2) 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 (3) a high protein formula particularly useful in those circumstances in which an oversupply of dietary protein might be recommended (i.e., pregnancy and lactation).
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PMID:The feeding of alcohol in liquid diets: two decades of applications and 1982 update. 675 24

Male and female, massively obese and nonobese, spontaneously hypertensive rat (SHR) which are hypersensitive to stress were kept under quiescent conditions; they were autopsied at 15 months of age. The blood pressure of the Obese/SHR plateaued at 166 mmHg versus 198 mmHg for the nonobese/SHR. The once massive thymi vanished in the Obese/SHR accompanied by greatly enlarged adrenal glands, pituitary basophilia, greatly elevated levels of adrenocorticotrophin, corticosterone, deoxycorticosterone, aldosterone, fatty liver, hyperlipidemia, and hyperglycemia. The Obese/SHR were hyperadrenocorticoid compared with their nonobese siblings and manifested a Cushingoid spectrum of degenerative changes (e.g., thin skin, hypertension, diabetes, kidney stones, and accelerated aging). The provision of a nonstressful environment is believed to have dampened the usual chronic hyperadrenocorticism and prolonged the lifespan of the Obese/SHR.
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PMID:Cushingoid pathophysiology of old, massively obese, spontaneously hypertensive rats (SHR). 682 32

Hypernatremic states, often the result of hypothalamic osmoreceptor dysfunction in humans, are sometimes accompanied by hyperlipemia. To investigate whether hypernatremia could cause hyperlipemia we induced hypernatremia in three groups of rats with their respective controls: Group A rats received hypertonic saline alone intragastrically; group B animals were pair-fed and tap water was substituted for hypertonic saline in the treated group; in group C the rats were again fed intragastrically with a liquid diet mixed with hypertonic saline. Rats receiving excess salt had mean serum Na+ concentrations exceeding 159 mmoles/l. While the serum triglyceride values were significantly higher in all hypernatremic rats, hepatic triglyceride content was greater only in group C rats (p less than .01). Serum free fatty acids and ketone bodies were also higher in group C rats (p less than .01) as compared to controls. These data suggest that hypernatremia by itself leads to hyperlipemia and a fatty liver.
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PMID:Hypernatremia induces hyperlipemia and a fatty liver. 684 93

Lipids of HDL (high density lipoproteins) and their subfractions (HDL2 and HDL3), and LCAT activity (lecithin: cholesterol acyltransferase) were determined in hepatobiliary diseases without severe hyperbilirubinemia (less than 10 mg/dl). The decrease in major lipid constituents (cholesterol and phospholipids) of HDL was mainly attributable to the decrease in those of HDL3, except in some liver diseases of acute or severe stage (acute hepatitis in an acute stage and hepatoma) which were accompanied with a simultaneous moderate decrease in those of HDL2 and in fatty liver which showed a preferential decrease in those of HDL2. The LCAT activity also decreased in several diseases. Some of the hepatobiliary diseases, on the contrary, showed an increase in HDL-triglycerides (mostly in HDL3 and in some diseases also in HDL2) which might participate to some extent in secondary hyperlipidemia in the liver parenchymal diseases, although they were the minor lipid constituents of HDL. From results that HDL3- but not HDL2-cholesterol levels significantly correlated with serum total protein, albumin and choline esterase, it was suggested that the decrease in large constituents of HDL, particularly of HDL3, is caused by hepatocellular dysfunction which causes inhibition of protein and lipid syntheses in the liver in most of the hepatobiliary diseases except for fatty liver which has a preferential decrease in HDL2 lipids.
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PMID:Changes in high density lipoproteins in patients with hepatobiliary diseases. Levels and lipid composition of HDL2 and HDL3 and LCAT reaction. 685 43

Regression of the main components of atherosclerotic leseions is compared with regression of other related pathological masses in the body, notably the fatty liver, the large abscess, the large thrombus, the tuberculous granuloma, the lipid implantation granuloma, an the at first reversible but later irreversible proliferation of tissues in response to certain hydrocarbons. The unique obstacles to the regression of advanced artheromata -- as compared to regression of pathological masses elsewhere -- are identified as a lack of early capillarisation, a dependence on evacuation by a very slow unidirectional filtration across an extremely dense and contracted tissue, a lack of an unending imigration of leucocytes for the phagocytic or lysosomal removal of large extracellular lipid pools, and the massive deposits of collagen, an insulating material of extremely long half-life that seems, in addition, to promote wall fragility and supra-plaque thrombosis. The origin and the fate of the myocyte proliferation in hyperlipemia-induced plaques is scrutinized; arguments are presented in favor of its regenerative rather than platelet-induced origin and in favor of the possibility that protracted hyperlipemia may induce the development of some regression-resistsant myocytic mutants. The special difficulties and pitfalls of regression research are analysed. The current conclusions from the most critical experimental studies to date indicate that incipient or young lesions are capable of significant regression, but there is as yet no evidence that advanced or complicated plaques will regress in any species.
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PMID:Overview of studies on regression of atherosclerosis. 701 65


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