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

Splanchnic metabolism was studied to quantify changes underlying the fatty liver, hyperlipemia, and hypoglycemia produced by ethanol. Four subjects fasted for 15 h were compared with five subjects fasted for 69 h under basal conditions and during continuous intravenous infusion of sufficient ethanol to give a concentration of 3-5 mM in arterial blood plasma. Splanchnic storage of fatty acids was estimated from the difference between uptake of FFA and secretion of derived products. Basal values for splanchnic uptake of FFA were twofold higher after the 69-h fast while splanchnic storage of fatty acids and production of ketone bodies increased threefold. Values for basal secreation into the blood of triglycerides derived from FFA were similar in the two groups. In both nutritional states, the fraction of FFA taken up in the splanchnic region oxidized to ketone bodies and to CO2 fell when ethanol was given because of preferential oxidation of ethanol to acetate, and the fraction esterified rose. However, systemic transport and splanchnic uptake of FFA fell with ethanol in subjects fasted 15 h, so that neither storage of triglycerides in splanchnic tissues nor secretion into the blood increased. In subjects fasted 69 h, ethanol increased transport of FFA and splanchnic storage of fat. In all but one subject it also increased secretion of triglycerides into the blood. The concentration of glucose in blood fell during ethanol infusion in all five subjects undergoing the 69-h fast. Mean splanchnic glucose production was maintained at about one-half of the pre-ethanol value, despite virtual cessation of splanchnic uptake of lactate and of those amino acids that are metabolized via malate. Quantitative estimates of extrasplanchnic metabolism suggest that enhanced formation of alpha-glycerophosphate from glucose, in addition to impaired hepatic gluconeogenesis, may contribute to ethanol-induced hypoglycemia in man.
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PMID:Effects of a 3-day fast and of ethanol on splanchnic metabolism of FFA, amino acids, and carbohydrates in healthy young men. 17 79

Case reports since 1957 implicate corticosteroids in excess of physiologic requirements as a cause of nontraumatic osteonecrosis. Both laboratory and clinical studies demonstrate marked alterations in lipid metabolism with hyperlipemia, fatty liver and systemic fat embolism. Intra-arterial infusion of fat produces embolic vascular obstruction, focal marrow necrosis and osteocytic death in the femoral head of the rabbit. Induced hypercortisonism in rabbits produces severe hyperlipemia, fatty liver, systemic fat emboli, terminal vascular obstruction in bone and associated areas of osteocytic death representing avascular necrosis. Osteoporosis develops without fracture. Histologic evidence of vasculitis, thrombosis, or microfracture is lacking. The specific biochemical pathway of corticosteroid lipid alterations is unknown.
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PMID:The role of fat embolism in the etiology of corticosteroid-induced avascular necrosis: clinical and experimental results. 63 8

Diabetes mellitus occurs in many animals species. However, only a few have been utilized in systematic studies designed to answer unsolved problems associated with the disorder in man such as molecular basis, pathogenesis of the vascular and neural lesions, and the roles of diet, exercise and obesity. Among the animal models available, rodents have been studied most thoroughly for a number of reasons: a) short generation time (sexually mature at about 3 mo of age, gestation time 21 days) and life-span is approximately 3 yr; b) hyperglycemia and/or obesity is known to be inherited in several species; c) environmental factors can be controlled easily in the laboratory because of small size; and d) economic considerations. The better-known rodent diabetes/obesity syndromes may be categorized as follows: 1) hyperglycemic with ketoacidosis, nonobese (Chinese hamster, South African hamster); 2) hyperglycemic with insulin hypersecretion, moderate obesity and may develop ketoacidosis (diabetic mouse (db/db), spiny mouse, sand rat); and 3) less pronounced hyperglycemia with hyperinsulinemia, insulin "resistance" and marked obesity (obese (ob/ob), yellow (Ay) and New Zealand obese (NZO) mice, and the Zucker "fatty" rat). The PBB/Ld mouse, described here in detail for the first time, is a new strain of mouse that also fits into the latter category. Members of this strain following maturity develop an obesity that is characterized by increasing cellularity of adipose tissue, increased serum immunoreactive insulin, reduced glucose tolerance, fatty liver, and hyperlipidemia. Therefore, this strain of mouse represents another model for study of adult onset obesity.
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PMID:Animal models of diabetes and obesity, including the PBB/Ld mouse. 77 Jan 97

A distict alcoholic withdrawal syndrome in chronic alcoholics cannot only be induced upon withdrawal of alcohol or dose reduction but also occurs upon continuous and long lasting consumption of larger quantities of alcohol. In the latter case we deal with an alcoholic predelirium which is characterized by simultaneous occurence of neurologic, vegetative and gastrointestinal disturbances as well as mental symptoms like anxiety, increased irritability and disturbance of sleep. In parallel to this alcoholic withdrawal syndrome from internal medical view a characteristic symptomatology can be observed in patients with chronic alcohol abuse. In most cases younger patients are concerned who, concomitantly with predelirant symptoms frequently display a labile hyperlipidemia and additional obesity, fatty liver, hyperlipidemia and often also hyperuricemia. Based on ten typical cases the combination of symptoms as described above is introduced. This combination can according to Feuerlein be defined as "alcohol-syndrome". The difficulties of diagnosis are shown because in many cases not the alcohol abuse but primarily vegetative and other functional disturbances dominate the clinical appearance. Additionally the pathogenetic connection between the described symptoms and alcohol abuse are discussed.
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PMID:[The "alcohol-syndrome" from internal medical view (author's transl)]. 86 89

A 25-year-old man was at first dermatologically suspected as suffering from Weber-Christian syndrome because of subcutaneous panniculitis, but his skin lesions disappeared completely during the course. Hyperlipidemia, disturbances in liver function, and leukemoid reaction became remarkable and he died of subarachnoid hemorrhage eleven months after onset. Necropsy revealed subarachnoid hemorrhage at the base of the brain, lipogranulomatous and inflammatory lesions in the upper lobe of the left lung, a remarkable fatty liver, splenomegaly, pericarditis, and foam cells in the spleen, liver, and bone marrow. A comparison with 57 autopsy cases of Weber-Christian syndrome reported in the literature showed our case to be an exceptional instance of Weber-Christian syndrome, if the present case is not to be regarded as a different disease entity.
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PMID:An unusual case which began with subcutaneous panniculitis followed by fever, severe hepatic involvement and hyperlipidemia. 87 Oct 84

The catabolism of chylomicrons was investigated in genetically obese rats and their nonobese littermates, and was compared with catabolism in older Sprague-Dawley rats with body weights similar to the obese rats and their younger controls. Labeled thoracic-duct lymph was collected from donor rats and the catabolism of the labeled chylomicrons was studied after a single intravenous injection or during steady intravenous infusion in unanesthetized, nonfasting, recipient rats. In the genetically obese rats clearances from the plasma of chylomicron triacylglycerol and cholesteryl ester were less than in their nonobese littermates. Fractional clearance rates were reduced for both triacylglycerol and cholesteryl ester but triacylglycerol turnover rate (mg min(-1)) was greater than controls. Chylomicron triacylglycerol clearance was more efficient than cholesteryl ester clearance so that radioactivity remaining in the plasma was relatively depleted in triacylglycerol. The large-bodied old Sprague-Dawley rats showed no reduction in clearance of chylomicron radioactivity in comparison with younger controls. These results suggest that hyperlipidemia in genetically obese rats may be due in part to an accumulation of chylomicron remnants in the plasma. Flotation characteristics of plasma lipoproteins in the obese rats were consistent with this interpretation. However, separate experiments showed that genetically obese, fasting rats also accumulated more triacylglycerol in the plasma after injection of Triton WR 1339. The enlarged plasma triacylglycerol pool appears to derive from a mixture of hepatic and intestinal triacylglycerol-rich lipoproteins which, together, overload their common removal mechanism. Addition of cholesterol to the diets of the obese rats exacerbated their hyperlipemia and hepatic steatosis whereas their nonobese littermates and the large-bodied Sprague-Dawley rats were unaffected.
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PMID:Catabolism of chylomicron triacylglycerol and cholesteryl ester in genetically obese rats. 90 8

Rats were fed for 24 days a liquid diet with ethanol as 36% of calories to produce hyperlipemia and hepatic steatosis. The catabolism of chylomicrons doubly-labeled in the triacylglycerol and cholesteryl ester moieties was studied in conscious rats after ingestion of their usual liquid diets with or without ethanol. A constant intravenous infusion of chylomicrons revealed a defect in chylomicron catabolism after chronic treatment with ethanol. The plasma clearance of chylomicron cholesteryl ester was impaired to a greater extent than clearance of chylomicron triacylglycerol. These findings are consistent with defective catabolism of chylomicron remnants, and suggest that the accumulation of chylomicron remnants in the plasma contributes to the development of increased post-prandial hyperlipemia and chronic hyperlipemia in association with excessive ethanol consumption.
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PMID:Effects of chronic ethanol consumption on the catabolism of chylomicron triacylglycerol and cholesteryl ester in the rat. 91 70

A model has been developed for the administration to rats and baboons of ethanol as part of a nutritionally adequate liquid diet. With this regimen, ethanol intake was much higher than with conventional procedures. All animals gained or maintained their body weight, and liver morphology was normal in the controls. Isocaloric substitution of carbohydrate by ethanol (36% of total calories in rats and 50% in baboons) resulted in the production of fatty liver in all animals, while the baboons also developed alcoholic hepatitis and cirrhosis with increased activities of serum glutamic oxaloacetic transaminase. Inebriation and manifestation of dependence on withdrawal of the diet were observed in baboons and quantitated in the rat. Chemical alterations produced by ethanol at the fatty liver stage were characterized by hyperlipemia, striking triglyceride accumulation in the liver, and enhanced activities of microsomal drug metabolizing enzymes, including the microsomal ethanol oxidizing system (MEOS). In showing that all aspects of liver injury observed in alcoholics can be reproduced in animals by the feeding of pure ethanol with an adequate diet, this study incriminates ethanol itself as a cause for the hepatic complications. This new experimental model is proposed as a tool for the study of the pathogenesis and treatment of alcoholic liver injury and dependence.
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PMID:Animal models of ethanol dependence and liver injury in rats and baboons. 94 46

Ethylism represents at the present time one of the most frequent etiological factors of primitive osteonecrosis of the femoral head. In relation to a case of osteonecrosis of the femoral head associated with multiple bone infarcts in a chronic alcoholic, also presenting recurring jaundice, alcohol-sensitive hyperlipidaemia, and moderate anaemia, the authors review the role of fatty embolisms in the formation of primitive osteonecrosis of the femoral head. These fatty embolisms may be the result of alcohol-induced hyperlipidaemia, possibly an associated pancreatic disorders, or in particular of hepatic steatosis. A systematic histological study of 10 recent unselected cases of primitive osteonecrosis of the femoral head confirmed the extreme frequency of such embolisms (8 cases out of 10).
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PMID:[Osteonecrosis, alcoholism and liver steatosis]. 112 80

To develop the prophylactics and the curatives for atherosclerosis, thyroxine derivative, CG-635, was assayed for its physiological activities in experimental atherosclerosis in rabbits fed with cholesterol. It was found that CG-635 possessed serum TC/TP value lowering activity (total cholesterol/total phospholipid) in normal and cholesterol fed rabbits for 3 weeks, and prevented the elevation of the value of cholesterol fed rabbits by daily injection for 7 weeks. CG-635 also depressed the hyperlipemia induced by cholesterol feeding, and its inhibitory effect was shown to be more marked on the increase of cholesterol than triglyceride, phospholipid and free fatty acid in serum. CG-635 did not, however, influence GOT, GPT and G-6-Pase activities in serum with increased cholesterol intake. From the histological findings it was proved that this compound prevented to a high degree the occurrence of atherosclerosis and fatty liver of cholesterol fed rabbits. Furthermore, it was recognized that thyroid hormone and the thyroid simulating hormone-like activities of CG-635 were much weaker than thyroxine, except for the action in the lipid metabolism.
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PMID:[Effect of d,l-alpha-methyl-3, 5, 3, 5-tetraiodothyronine ethylester hydrochloride (CG-635) on experimental hypercholesterolemia and atherosclerosis in rabbits (author's transl)]. 117 Oct 31


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