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

Almost all of risk factors for arteriosclerosis and coronary heart disease identified in population studies are overrepresented in diabetes. Of these risk factors, plasma lipids and lipoproteins are the target for altered dietary habits, particularly regarding fat. Such an alteration must be qualified with an understanding of the relationship between diabetes mellitus and lipoprotein metabolism and evidence of a favorable outcome of a fat-modified diet on this relationship. In seeking a revision of the current dietary fat recommendations of the American Diabetes Association, we have addressed five major questions. Is the serum lipid or lipoprotein concentration in diabetes different from that of the nondiabetic population? Are the familial or genetic forms of hyperlipidemia coinherited and/or overrepresented in diabetic subjects? What is the mechanism of the lipid/lipoprotein disorder in diabetes, and to what extent could it be related to the diabetic metabolic milieu? What is the effect of antidiabetic treatment on plasma lipids and lipoprotein metabolism? What evidence is there that a modified-fat diet could exert favorable benefits over and above what could be achieved by optimal antidiabetic therapy? This article outlines the revised dietary fat recommendations of the American Diabetes Association Nutrition Task Force and their rationale.
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PMID:Polyunsaturated and saturated fat, cholesterol, and fatty acid supplementation. 328 63

The production and catabolism of very low density lipoprotein triglycerides (VLDL-TG) were determined in 11 index patients with primary hypertriglyceridemia and in their 70 first-degree relatives. In the probands the mean value for VLDL-TG production rate was twice normal, and the mean fractional catabolic rate (FCR) was reduced to 50% from normal. A similar kinetic pattern was also observed in most hypertriglyceridemic relatives. In the normotriglyceridemic relatives the mean values of both kinetic parameters were comparable to those of controls. No kinetic differences were observed between families with familial hypertriglyceridemia, familial combined hyperlipidemia, or genetically unclassified hypertriglyceridemia (all diagnosed by lipoprotein phenotypes). Thus, no explanation for the phenotypic differences between the two forms of familial hyperlipoproteinemia was found in plasma VLDL-TG metabolism. When the families were grouped according to the VLDL-TG production rate of the proband, there was no significant difference between the VLDL-TG production rates of relatives of "overproducer" probands and relatives of the probands with normal VLDL-TG production rate. In contrast, relatives of low FCR probands had significantly lower mean FCR than the relatives of probands with a normal FCR. This difference in FCR was present both in hypertriglyceridemic and normotriglyceridemic relatives. These results suggest that the catabolism (lipolysis) of VLDL-TG is under genetic control, whereas the VLDL-TG production rate is mainly related to obesity. It is likely that hypertriglyceridemia often develops on the basis of VLDL overproduction in individuals who have a genetically low VLDL triglyceride removal (lipolytic) capacity.
Arteriosclerosis
PMID:Very low density lipoprotein triglyceride metabolism in relatives of hypertriglyceridemic probands. Evidence for genetic control of triglyceride removal. 337 19

There were 72 patients (19 with hepatic failure, 10 with fulminant hepatitis, eight with paraquat poisoning, eight with rheumatoid arthritis, five with myasthenia gravis, four with hyperlipidemia, four with systemic arteriosclerosis including brain infarction, three with pemphigus vulgaris, two with multiple myeloma, two with systemic lupus erythematosus, two cases non-specific Ig-G antibody, two cases medication with an anticancer drug, one with multiple sclerosis, one with Crohn's disease with amyloid kidney and one with chronic myeloblastic leukemia) treated by plasma exchange in the Kidney Center, Tokai University School of Medicine from Jan. 1983 to Dec. 1986. We performed plasma exchange using fresh frozen plasma in 40 cases and Lactate-Ringer's solution containing albumin (4.0-5.0%) in 20 cases as the replacement fluid. In 17 cases, we performed double filtration plasma exchange with the recycle system and no replacement fluid. Although PE therapy did not constitute a basic therapy for hyperlipidemia, pemphigus vulgaris, rheumatoid arthritis, myasthenia gravis, and systemic lupus erythematosus, it was effective in relieving severe clinical symptoms. At the present time, conventional plasma exchange does not improve the survival rate of patients with hepatic failure and fulminant hepatitis. Developments of a new artificial liver support apparatus and identity of many toxic substances in hepatic failure are necessary. No hypotension, hypovolemic shock or other significant complications were experienced.
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PMID:Clinical reports on plasma exchange in the Kidney Center, Tokai University School of Medicine. 344 83

An inherited metabolic disorder in a strain of New Zealand White rabbits, characterized by marked hypercholesterolemia (394 +/- 100 mg/dl), with moderately elevated or normal triglyceride levels is described. Low density lipoprotein (LDL), intermediate density lipoprotein (IDL) and very low density lipoprotein (VLDL) cholesterol levels were increased. VLDL and IDL, and to a lesser extent LDL, had increased free cholesterol and esterified cholesterol content, and triglyceride content was reduced. Kinetic studies with 131I and 125I-labelled rabbit lipoproteins showed a marked increase in production rates of VLDL apo B and LDL apo B. LDL cholesterol levels were directly related to LDL apo B production rate (r = 0.938, p less than 0.001). Both in hypercholesterolemic and normal rabbits injected with labelled VLDL, the specific activity-time curves of VLDL apo B and LDL apo B did not intersect, indicating that LDL apo B was in part derived from sources other than VLDL. No defect was demonstrated in receptor-mediated catabolism of LDL by cultured skin fibroblasts from hyperlipidemic animals. The fractional catabolic rate of LDL apo B was subnormal, but increased when the expanded LDL apo B pool size was reduced by exchange transfusion; the low fractional catabolism may therefore be attributable, at least in part, to saturation of LDL receptors consequent upon the increased pool size of LDL. The hyperlipidemia in this strain of rabbits may be unique in that the underlying mechanism appears to be overproduction of VLDL and LDL.
Arteriosclerosis
PMID:Hereditary hyperlipidemia in the rabbit due to overproduction of lipoproteins. I. Biochemical studies. 357 20

A genetically determined hyperlipidemic strain of New Zealand White rabbit that has features in common with combined familial hyperlipidemia in humans has been identified. The morphologic findings in a few animals fed a normal chow diet are reported. These consisted of macroscopically visible aortic intimal elevations found in the greatest number in the descending thoracic aorta. The plaques showed the presence of a cell population consisting of modified smooth muscle cells and lipid-laden macrophages. The lesion bases were necrotic and acellular, and some showed the presence of dystrophic calcification. Scanning electron microscopy revealed numerous monocytes attached to the endothelium. Endothelial defects were common, and these were filled with swollen and "ruffled" macrophages. Transmission electron microscopy confirmed the presence of lipid-laden cells penetrating between adjacent endothelial cells. These findings resemble those reported in a number of different animal species after dietary induction of hyperlipidemia. This strain is a useful new model for the study of atherogenesis.
Arteriosclerosis
PMID:Hereditary hyperlipidemia and atherosclerosis in the rabbit due to overproduction of lipoproteins. II. Preliminary report of arterial pathology. 357 21

A child showed a type IIb lipoprotein pattern and triglyceride-enriched cutaneous xanthomas before 1 year of age. The proband and 9 of 18 relatives had elevated plasma levels of low density lipoprotein (LDL) B protein; of these nine relatives, four had elevated LDL of increased density while five had elevated LDL of normal density. Compared with normal LDL, LDL of increased density had less cholesteryl ester and free cholesterol, more apolipoprotein B and triglyceride, and a lower molecular weight and flotation rate (Sf degrees). Patients with LDL of increased density had higher mean plasma levels of triglycerides, very low density lipoproteins, and intermediate density lipoproteins, but lower levels of high density lipoproteins than those with elevated LDL of normal density. Multiple lipoprotein patterns in the father's family suggested the presence of familial combined hyperlipidemia (FCH). The mother of the proband and two of her relatives had type IIa lipoprotein patterns and tendon xanthomas, compatible with familial hypercholesterolemia (FH). High affinity binding, internalization, and degradation of 125I LDL in cultured fibroblasts from the proband and his mother were reduced two- to threefold compared with normal cells, while LDL receptor activity in the proband's father was normal. This unusual proband has apparently inherited both FCH and FH.
Arteriosclerosis
PMID:Hyperapobetalipoproteinemia in a kindred with familial combined hyperlipidemia and familial hypercholesterolemia. 359 67

Several parameters of lipoprotein metabolism were examined in 38 men with primary hypertriglyceridemia (phenotype IV). Family investigation showed that 17 men had familial combined hyperlipidemia (FCH), seven had familial hypertriglyceridemia (FHT), and 14 had unclassified hypertriglyceridemia (UNC). In all three groups, plasma high density lipoprotein (HDL) cholesterol and the concentrations of apolipoprotein A-I and A-II were decreased, and apolipoprotein B was increased, each to the same extent. These results are compatible with an increased risk of cardiovascular disease in both FCH and FHT patients. The mean concentration of LDL cholesterol and the ratio of LDL to HDL cholesterol were significantly higher in FCH subjects, which could explain their increased risk. Postheparin lipoprotein lipase and hepatic lipase were the same in both groups. Determination of apolipoprotein C composition, which may modulate lipoprotein lipase activity, did not reveal any abnormalities in the different groups. In both FCH and FHT, the mean turnover rate of plasma triglycerides was almost twice normal, indicating that overproduction of plasma triglyceride plays an important role in both disorders. However, there was an overlap with normal controls, indicating impaired triglyceride removal in some subjects. The underlying mechanism of hypertriglyceridemia in FCH and FHT therefore seems to be heterogeneous.
Arteriosclerosis
PMID:Plasma lipoproteins, apolipoproteins, and triglyceride metabolism in familial hypertriglyceridemia. 372 96

Apolipoprotein E polymorphism is responsible for the existence in the population of six apo E phenotypes determined by three alleles acting at a single gene locus. We have previously reported an enrichment in the epsilon 2 allele and the E2-bearing phenotypes in an unselected sample of subjects with primary hyperlipidemia consisting mainly of endogenous hypertriglyceridemia (Type IV). A study was carried out on 214 Type IV hypertriglyceridemic subjects to determine whether there was the same distribution in subjects with hyperapobetalipoproteinemia as in those without. The study showed that the relative enrichment in the epsilon 2 allele was associated only with Type IV subjects without hyperapobetalipoproteinemia. Since hyperapobetalipoproteinemia is a presumed marker for familial combined hyperlipidemia (FCHL), this finding may provide further evidence that FCHL and familial hypertriglyceridemia, both associated with a Type IV lipoprotein pattern, are truly separate disease entities.
Arteriosclerosis
PMID:Apo E allele frequency in primary endogenous hypertriglyceridemia (type IV) with and without hyperapobetalipoproteinemia. 386 49

A protein band having the same migration as apolipoprotein (apo) B-48 was observed by SDS electrophoresis in the plasma very low density lipoprotein (VLDL) from 14 Type IV and three Type III hyperlipoproteinemic subjects and from six normal fasting subjects. The VLDL from five Type IV, three Type III, and one normal subject were separated into two subfractions, retained and nonretained, by immunoaffinity chromatography on monoclonal anti-apo B-100 Sepharose. Based on results of electrophoresis and radioimmunoassay, we have concluded that these two fractions represent apo B-48 and apo B-100 lipoproteins that we have named apo B-48 and apo B-100 VLDL. When compared to their respective apo B-100 VLDL, the apo B-48 VLDL from either Type III or Type IV was principally enriched in total lipids, in apo E, and had an electrophoretic migration similar to chylomicrons. This suggests that apo B-48 VLDL has the same origin (i.e., intestinal) in the two disorders. Both apo B-48 and apo B-100 VLDL were enriched in cholesteryl ester (CE) and depleted in triglyceride (TG) in Type III; however, both fractions were rich in TG and poor in CE in Type IV and in normal subjects. In addition, compared to their respective apo B-100 VLDL, the apo B-48 fraction was enriched in CE in Type III and in TG in Type IV. We conclude that, despite a possible similar origin for apo B-48 VLDL in Type III and in Type IV subjects, the composition of apo B-48 VLDL is variable and the CE/TG ratio is more characteristic of the type of hyperlipidemia than of the particular VLDL subfractions.
Arteriosclerosis
PMID:Apolipoprotein B-48 and B-100 very low density lipoproteins. Comparison in dysbetalipoproteinemia (type III) and familial hypertriglyceridemia (type IV). 397 78

In order to evaluate the prevalence of common and/or internal carotid stenoses together with metabolic abnormalities in dementia nineteen patients were investigated. Dementia and differential diagnosis between Alzheimer type (DAT) and multi-infarctual (MID) dementia were performed on the basis of Computerized Tomography scan, behavioural anamnesis, neurological and neuropsychological examinations. Eight patients were diagnosed as MID and 11 as DAT. Noninvasive study of neck arteries was performed in supine position by a Duplex Scanner, able of detecting a wide range of stenosis, even when very mild. Arterial hypertension, hyperlipidemia, diabetes and high hematocrit level were present in both groups, although to a higher extent in MID (p 0.05). Results from Duplex Scanner demonstrate 12 vascular stenoses 16-49% and one between 50-99% (13/76), being vascular abnormalities equally distributed among DAT and MID patients. These data suggest that patients with metabolic abnormalities and arteriosclerosis can develop dementia not necessarily of vascular type. On the other hand, MID patients do not present higher number of stenosis as compared to DAT, indicating that vascular disease of carotid arteries is not prominent in the clinical context of dementia.
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PMID:Non invasive study of carotid arteries by echo-doppler and metabolic abnormalities in patients with dementia. 402 28


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