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

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

The purpose of the studies was to show the relationships between secondary hyperlipaemia and post-vaccination nephritis induced by lapinized vaccine with additional infection with the living virus of pig plague and the virus itself. CT, CF, LT, FFA and LP fractions were studied in the serum of blood taken from the vena cava cranialis from piglets weighing 30 - 40 kg, of the large white breed. In the animals of group 1, in the initial series a, series b - immunized with lapinized vaccine, series c - immunized and infected with virulent viruses, and also in group 2d - infected with the virus itself, the concentration of the lipids mentioned above was studied by the methods used elsewhere. The kidneys of the animals in series c and group 2d were examined histopathologically, staining them with h.e. and oil red solution neutral to fats. Multifocal inflammation reaction with the presence of fine-grained lipids were found. Particularly in group 2d the pathomorphological image, by its intensiveness and extensiveness pointed to severe inefficiency of kidneys. In series b and c of group 1a linear increase in the concentration of the lipids studies was found, as compared with series a. Hyperlipaemia was most distinctly marked in group 2d. This leads to the conclusion that hyperlipaemia may occur in severe viral nephritis. The extention of hyperlipaemia depends on the degree of the organ damage, which was more advanced in group 2d than in series c of group 1. Vaccination with lapinized vaccine caused a moderate increase of lipids in blood serum, which oscillated on the line of significance.
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PMID:[Hyperlipidemia in swine immunized with lapinized vaccine and live swine plague virus]. 653 93

The results of plasma lipid and lipoprotein analysis in two related patients, brother (R.U.) and sister (R.R.) with analbuminemia, and three first-degree relatives (parents and sister) are reported. Both patients showed a remarkable increase in cholesterol and phospholipid levels, and there was a corresponding increase in serum apo B and apo A-I. This hyperlipidemia is due to a selective increase in LDL and HDL concentrations. R.U. showed an increase in both HDL2- and HDL3-cholesterol, R.R. only in HDL3-cholesterol. VLDL concentration was reduced in R.U. and normal in R.R. The plasma lipoprotein electrophoretic pattern did not correspond to any of the phenotypes in Fredrickson's classification. Composition of the different lipoprotein fractions was normal in the patients and family members. Serum FFA level in R.R. was very low. An increase in the plasma protein fractions, particularly the transport fractions, was confirmed in both patients. The possible pathophysiology of the hypercholesterolemia in these patients is discussed. Unlike other reported cases, clinical signs of atherosclerotic complications were absent.
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PMID:Characterization of hyperlipidemia in two patients with analbuminemia. 685 Nov 39

Resistance to both insulin and glucagon have been considered as possible causes of primary hypertriglyceridemia. In the present research, we have compared insulin and glucagon secretion in five hyperlipidemic patients with familial dysbetalipoproteinemia with five normolipidemic control subjects matched for age, sex and adiposioty. Plasma insulin and glucagon concentrations mesaured during standard oral glucose tolerance and arginine infusion tests were similar in the two groups. Blood glucose fell transiently in the controls, but not in the patients, during the Himsworth test (100 g glucose orally plus 0.05 U insulin per kg body weight intravenously). There were no significant differences in plasma FFA concentrations and responses during all tests between the groups. The percentage reduction in plasma triglyceride concentration during infusion of arginine was similar in the two groups. These results suggest that the patients with familial dysbetalipoproteinemia were slightly less insulin sensitive than the controls. However, primary insensitivity to glucagon or insulin does not appear to be fundamental to the pathogenesis of hyperlipidemia in familial dysbetalipoproteinemia.
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PMID:Pancreatic alpha and beta cell function in familial dysbetalipoproteinemia. 700 Jun 52

Hyperlipemia occurs during pregnancy. The present study deals with lipid metabolism in the female by comparing the response of the pregnant with that of non-pregnant females to a lipid loading test with 10% Intralipid given intravenously. The results were: (i) Exogenous and endogenous triglycerides (TG) were significantly higher inthe pregnant group. (ii) The K2 value was significantly lower in the pregnant group. (iii) The level of FFA in the non-pregnant group rose rapidly 5 min after Intralipid load. In contrast, the pregnant group showed a gradual rise which reached a maximum one hr after administration of Intralipid. The delay of the lipid metabolism during pregnancy might be one of the reason of hyperlipemia.
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PMID:Fat tolerance test in pregnancy: Intralipid loading test. 731

In order to assess the impact of coronary disease on sequential physiological reactions to stress, this study compares 21 post myocardial infarction patients with 21 matching non-coronary subjects. In each group, levels of phospholipids, triglycerides, cholesterol, FFA, alpha-, beta, pre-beta-lipoproteins and the ratio cholesterol/triglycerides are assessed, six times consecutively in a timespan of 2 hours. Concomitantly, two stressful situations are induced: the first stress is catheterization, the second is a film implementing either a focused-or diffused anxiety. Phospholipids react essentially to catheterization stress. While the ratio cholesterol/triglycerides turns out to be sensitive to psychological stress, neither cholesterol nor triglycerides alter individually when psychological stress is present. Throughout the experiment, levels of beta-lipoproteins very significantly in time and with respect to the theme of the film attended; coronary patients do not show the same sequential variations as normal subjects do. Variations in alpha-lipoproteins differentiate coronary from normal subjects. Levels of FFA vary according to the nature of the film attended and differ in normal and coronary subjects: extreme values are observed in normal subjects rather than coronary patients. Hyperlipidemia, as a reaction to stress, is a process interlinked with many factors, each increasing the liability of coronary disease.
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PMID:[Temporal evolution of lipids in reaction to various stressors in coronary and non-coronary subjects (author's transl)]. 745 63

Transgenic mice were generated with different levels of human apolipoprotein C1 (APOC1) expression in liver and skin. At 2 mo of age, serum levels of cholesterol, triglycerides (TG), and FFA were strongly elevated in APOC1 transgenic mice compared with wild-type mice. These elevated levels of serum cholesterol and TG were due mainly to an accumulation of VLDL particles in the circulation. In addition to hyperlipidemia, APOC1 transgenic mice developed dry and scaly skin with loss of hair, dependent on the amount of APOC1 expression in the skin. Since these skin abnormalities appeared in two independent founder lines, a mutation related to the specific insertion site of the human APOC1 gene as the cause for the phenotype can be excluded. Histopathological analysis of high expressor APOC1 transgenic mice revealed a disorder of the skin consisting of epidermal hyperplasia and hyperkeratosis, and atrophic sebaceous glands lacking sebum. In line with these results, epidermal lipid analysis showed that the relative amounts of the sebum components TG and wax diesters in the epidermis of high expressor APOC1 transgenic mice were reduced by 60 and 45%, respectively. In addition to atrophic sebaceous glands, the meibomian glands were also found to be severely atrophic in APOC1 transgenic mice. High expressor APOC1 transgenic mice also exhibited diminished abdominal adipose tissue stores (a 60% decrease compared with wild-type mice) and a complete deficiency of subcutaneous fat. These results indicate that, in addition to the previously reported inhibitory role of apoC1 on hepatic remnant uptake, overexpression of apoC1 affects lipid synthesis in the sebaceous gland and/or epidermis as well as adipose tissue formation. These APOC1 transgenic mice may serve as an interesting in vivo model for the investigation of lipid homeostasis in the skin.
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PMID:Hyperlipidemia and cutaneous abnormalities in transgenic mice overexpressing human apolipoprotein C1. 942 76

A line of transgenic rats (heterozygotes) carrying a chimeric gene comprising a regulatory portion of murine whey acidic protein and a structural portion of human GH (hGH) genes developed severe obesity with age. To characterize physiological mechanisms that lead to fat accumulation, an array of parameters related to obesity were studied. Blood hGH levels were continuously low, endogenous rat GH secretion was suppressed, and the pulsatility in peripheral GH levels was absent. Plasma glucose, insulin, triglyceride, and FFA levels in the male transgenic rats significantly exceeded those in nontransgenic littermates at 12 and 17 weeks, but not at 7 weeks, of age. All symptoms except hyperlipidemia were restored to normal by treatment with an antidiabetic agent, thiazolidinedione (troglitazone), for 1 week from 17 weeks of age. As phenotypic expression of obesity was already evident before aberration of physiological parameters, it was assumed that animals had a condition in which obesity or hyperlipidemia caused hyperinsulinemia. Gene expression and enzymatic activity of lipoprotein lipase in the adipose tissue in the transgenic rats were not different from those in normal rats. In contrast, the gene expression level of glycerol-3-phosphodehydrogenase was markedly elevated, suggesting that glycerol synthesis was much enhanced in the adipocytes of the transgenic rats. In an i.p. glucose tolerance test, the transgenic rats were not hyperglycemic at 7 weeks of age; however, the animal became hyperglycemic at 15-17 weeks of age. Finally, treatment with recombinant hGH for 1 week to produce pulsatile secretion reduced the size of epididymal and kidney fat pads and restored normal weight gain. These observations suggest that continuously low peripheral GH levels with the lack of pulsatile secretion resulted in obesity and noninsulin-dependent diabetes mellitus.
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PMID:Obesity and insulin resistance in human growth hormone transgenic rats. 964 76

A 71-year-old woman was admitted to our hospital because of severe hypertriglyceridemia. The patient had a 26-year history of non-insulin-dependent diabetes mellitus and hyperlipidemia (T-chol 300 mg/dl, TG 300 mg/dl). She was treated with sulfonylurea and clofibrate. Seven years before admission, she had undergone a radical mastectomy for cancer of the left breast. After the operation, she had received tamoxifen and fluorouracil. One month before admission, she had marked hypertriglyceridemia (triglyceride 2,106 mg/dl). After discontinuation of tamoxifen and fluorouracil, her serum triglyceride level decreased to 372 mg/dl; when tamoxifen was given again, it increased to 581 mg/dl, and her hepatic triglyceride lipase activity decreased from 0.228 to 0.164 mumol FFA/ml/min. Apolipoprotein E phenotype was wild type E3/3. The concentration of sex-hormone-binding globulin increased from 110 to 130 nmol/l. These changes associated with tamoxifen treatment were similar to those seen after administration of estrogen. Tamoxifen, an anti-estrogen, has been used as adjuvant therapy in cases of estrogen-receptor-positive breast cancer. Tamoxifen has some weak estrogenic activity. The tamoxifen-induced hypertriglyceridemia seen in this case was an effect of its estrogenic action.
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PMID:[Severe hypertriglyceridemia induced by tamoxifen]. 1006 74

Insulin exerts wide variety of biological effects through interaction with its specific receptor, which belongs to a large family of receptor tyrosine kinases. The activated insulin receptor phosphorylates the intracellular substrate IRS protains, which then bind various signalling molecules that contain Src homology 2 domains. The first downstram molecule that was shown to associate with IRS protains is PI3-kinase. PI3-kinase contributes to a wide variety of biological actions. Both Akt(PKB), a serine-threonine kinase with a PH domain, and atypical PKC(PKC zeta, PKC lambda) have been implicated as downstream effectors of PI3-kinase. Insulin resistance contributes to the pathogenesis of NIDDM. Both primary, genetically, and secondary, environmentally factors are important for insulin resistance. The secondary factors include hyperglycemia, hyperlipidemia, obesity, TNF alpha, FFA(free fatty acid).
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PMID:[Insulin signalling system and mechanism of insulin resistance]. 1070 48


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