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 serum-lipids were determined in 31 hyperlipemia patients before and after treated with the mixture of Acanthopanax senticosus and Elscholtzia splendens. While the mean value of serum beta-lipoprotein decreased from 902 +/- 228 mg/dl to 608 +/- 189 mg/dl (P less than 0.001), the mean value of HDL-C increased from 52.6 +/- 12.5 mg/dl to 61.2 +/- 15.4 mg/dl (P less than 0.001). Thus the ratios of HDL-C to total cholesterol (HDL-C/TC) and to LDL-C (HDL-C/LDL-C) increased significantly, the arteriosclerosis index (AI) decreased significantly. The results indicate that the mixture of Acanthopanax senticosus and Elsholtzia splendens could improve the lipid-metabolism in hyperlipemia patients so that it might play a good role in preventing or alleviating arteriosclerosis.
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PMID:[Effect of a mixture of Acanthopanax senticosus and Elsholtzia splendens on serum-lipids in patients with hyperlipemia]. 237 99

To test the hypothesis that endurance training is associated with a decreased lipemia after a high fat meal, 16 young men [22 to 34 years old, nine of whom were trained (T) and seven of whom were untrained (UT)] were recruited. T ran greater than 30 or biked greater than 100 miles a week, while UT had been sedentary for at least the preceding 3 months. Daily caloric intake and daily caloric expenditure during exercise were 35% and 704% greater, respectively, in T than in UT. VO2max was 31% greater, while percent body fat was 36% lower in T than in UT. Dietary composition and body height and weight were similar. After a fasting blood sample was taken, the men ate a high fat meal (approximately 56% of total calories as fat in 1100 kcal adjusted to body weight), and additional blood samples were taken hourly for 8 hours. Fasting lipids were similar. Postprandial peak triglyceride (TGmax), percent TG increase (%TGI), and total lipemic response (TLR, the area under the lipemia curve in excess of fasting TG) were 42%, 54%, and 75% greater, respectively, in UT vs. T. Stepwise regression analysis showed that the same three-variable model (training status, fasting TG, and VO2max) described the variation in TGmax (R2 = 0.97), %TGI (R2 = 0.75), and TLR (R2 = 0.92). Furthermore, this same analysis showed that after adjustment for fasting TG and VO2max, the UT group had a significantly greater postprandial lipemia whether expressed as TGmax (p less than 0.0001), %TGI (p = 0.0002), or TLR (p = 0.0002).(ABSTRACT TRUNCATED AT 250 WORDS)
Arteriosclerosis
PMID:Hyperlipemic response of young trained and untrained men after a high fat meal. 249 84

Familial dyslipidemic hypertension (FDH) is a syndrome recently described from sibships selected for early familial hypertension and found to have one or more of three fasting lipid abnormalities [high triglycerides, low high density lipoprotein (HDL) cholesterol, high low density lipoprotein (LDL) cholesterol]. In further analyses of these same 131 hypertensive subjects, apolipoprotein A-I and B, fasting plasma insulin (adjusted for body mass index), and detailed anthropometrics were different in two subgroups of FDH. Of 63 FDH patients, 19 met the criteria for familial combined hyperlipidemia (FCHL); 44 did not, but still had high triglyceride and/or low HDL cholesterol levels. When compared to 20 normolipidemic hypertensive patients, the 19 hypertensive patients with FCHL had 196% higher very low density lipoprotein cholesterol (p = 0.0001), 33% higher apolipoprotein B (p = 0.0002), smaller LDL particles (p = 0.007), and 73% higher fasting insulin (p = 0.003), but no significant differences in body mass index or skinfold thicknesses. The other 44 FDH patients without FCHL had 33% lower HDL (p = 0.0001), with only 8% lower apolipoprotein A-I levels (p = 0.20); significantly higher subscapular skinfolds (p = 0.02), weights (p = 0.002), body mass index (p = 0.006), knee widths (p = 0.0007), and wrist circumferences (p = 0.0009); smaller, denser LDL subfractions (p = 0.001); and increased apolipoprotein B levels (p = 0.01) compared to the normolipidemic hypertensive group. Increased fasting insulin levels were similar to the normolipidemic group and significantly lower than the FCHL group after adjustment for body mass index, suggesting a relationship between obesity and fasting insulin levels only in the non-FCHL group. We conclude that FDH consists of at least two subgroups: 1) FCHL with high apolipoprotein B, small LDL particles, and increased fasting plasma insulin levels, and 2) a less well-defined residual having upper central obesity with low HDL cholesterol and high triglyceride levels. Elevated insulin levels found in both groups, but possibly originating through different physiological mechanisms, may provide the pathophysiological connections between dyslipidemia, obesity, and hypertension.
Arteriosclerosis
PMID:Apolipoprotein, low density lipoprotein subfraction, and insulin associations with familial combined hyperlipidemia. Study of Utah patients with familial dyslipidemic hypertension. 249 19

In this paper, we studied the effect of elastase on aminonucleoside (AN) nephrosis which is considered a model of focal glomerular sclerosis (FGS). Elastase is an enzyme which disintegrates elastin, discovered by Balo, and used in the treatment of arteriosclerosis and hyperlipidemia. It has also been known to improve metabolism of acid mucopolysaccharides, so, this study focused on metabolic improvement. Three groups of male Sprague-Dawley rats were studied and observed at regular intervals; 30, 60, 90 days. The ANE group (AN + elastase) was administered one shot of AN (10 mg/100 g B.W.) during the test interval, while elastase (5 mg/kg B.W.) was injected 5 days/week for the entire test interval. The AN group was administered one shot of AN only. The third group was a control (C). The following results were observed: (1) Focal segmental hyalinosis and sclerosis (FSHS); ANE group was weaker than AN group. (2) Other significant qualifying glomerular changes (vacuolar change and hyaline droplets of the epithelial cells, adhesion, and foam cells); ANE group was weaker than AN group. (3) Anion loss in GBM was shown by a lack of colloidal iron staining under light microscopy, and by a lack of PEI particles under electron microscopy; there was significantly less anion loss with ANE group, than with AN group. The findings suggest that elastase has an affect on the metabolism of acid mucopolysaccharide and collagen in sclerotic lesion, and may restrain the progress of amino-nucleoside nephrosis.
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PMID:[The effect of the elastase on aminonucleoside nephrosis]. 253 42

In the United Kingdom, about 5% of patients with familial hypercholesterolemia (FH) have a detectable deletion or rearrangement of part of the LDL-receptor gene, which results in the detection of shorter or abnormally sized fragments of the LDL-receptor gene in a Southern blot hybridization. This gene deletion can be used for following the inheritance of the defective gene and for diagnosis in the families of these individuals. In the families of the remaining patients, diagnosis may be possible using linked restriction fragment length polymorphisms (RFLPs) detected with the LDL-receptor probe. There are now 10 common RFLPs of the LDL-receptor gene, with variable sites in the 3' half of the gene. Over 80% of patients are heterozygous for at least one of these RFLPs, and, therefore, RFLPs are potentially informative for DNA diagnosis. For a fetus at risk of homozygous FH, antenatal diagnosis may also be possible using these methods. However, family studies require samples to be available from affected or unaffected relatives of the patient, and this limits the applicability of the tests. For some mutations, the base-pair change causing the defect in the LDL receptor itself creates or destroys a site for a restriction enzyme. Such "mutation-specific" RFLPs could be used for population screening, but, so far, such use has only been reported for the FH mutation common in Lebanon. In the future, it may be possible to develop mutation-specific oligonucleotide probes for the diagnosis of FH. These would be appropriate for screening populations or patients with hyperlipidemia. This information may also be useful if different mutations require different therapeutic strategies.
Arteriosclerosis
PMID:Gene probes in diagnosis of familial hypercholesterolemia. 256 21

To assess the extent to which endothelial cell (EC) structure is modified by hyperlipidemia and by the formation of intimal plaques, we undertook a quantitative ultrastructural study of aortic EC of cynomolgus monkeys after 3 or 6 months on an atherogenic diet. We compared EC in lesion-free areas (LFA) with EC overlying focal discrete foam cell accumulations (FDA) or covering multilayered confluent plaques (MCP). There was a 15% increase in cross-sectional lumen surface profile length over FDA or MCP compared to LFA (p less than 0.005) corresponding to the bulging contours of immediately underlying foam cells. There was, however, no increase in the number of EC per unit of surface area (26.2 +/- 4.47 per 10(4) mm2 for LFA and 26.0 +/- 4.22 for FDA) or, on cross-section, per 100 microns length of underlying internal elastic lamina (8.79 +/- 2.42 for LFA, 8.26 +/- 2.01 for MCP). Nor did the number of surrounding cells contacted by each cell over LFA or MCP differ from normolipemic controls (6.56 +/- 0.85 for LFA and 5.58 +/- 0.86 for MCP). Most ECs were markedly attenuated over lesions, and while the extent and complexity of lateral contact regions between adjacent EC was diminished, the number and complexity of basilar projections was greatly increased. These structures extended among the intimal foam cells to insert on the internal elastic lamina or on intimal matrix fibers, resulting in a 2.7-fold increase in the length of the abluminal portion of the EC profile. The perimeter of the transverse EC profiles was thereby increased from 41.4 +/- 2.12 microns in LFA to 82.2 +/- 5.21 microns over MCP (p less than 0.0001). Polarization of EC in the direction of flow diminished as lesions developed. The ratio of length to width, as well as the standard deviation of the ratio, decreased from 3.51 +/- 3.92 in LFA to 2.35 +/- 0.25 over MCP, due mainly to increases in the proportion of the cell perimeter exposed to the lumen. Lesion localization bore no relationship to the orientation of EC in corresponding locations in the normolipemic controls or in LFA immediately adjacent to plaques. Organelles of EC in hyperlipidemic animals showed features suggestive of increased metabolic activity in all regions, and stress filaments were increased in the EC attenuated over lesions. There was no evidence of EC degeneration, necrosis, or sloughing regardless of lesion location, size, or complexity.
Arteriosclerosis
PMID:Preservation and structural adaptation of endothelium over experimental foam cell lesions. Quantitative ultrastructural study. 259 66

The JCR:LA-corpulent rat is an obese, hyperlipidemic, hyperinsulinemic strain that is atherosclerosis-prone and develops myocardial lesions. The hyperlipidemia is due to elevated plasma levels of a large relatively triglyceride-rich very low density lipoprotein (VLDL). Both corpulent and lean male and female rats were studied. Postheparin lipid clearance and apparent hepatic secretion rate after Triton WR1339 inhibition of lipoprotein lipase were determined. The concentrations of cholesterol and cholesteryl esters were not significantly altered by either treatment. Triglycerides showed rapid postheparin clearance in corpulent rats. The apparent hepatic secretion rate was markedly higher in corpulent male rats than in lean male rats, and the rate in corpulent females was again higher, reflecting the higher serum triglyceride concentrations in corpulent female rats. The relative secretion rate of C:48 triglyceride molecular species was lower than that of the C:50 to C:56 species, while the postheparin clearance of C:48 triglyceride molecular species was impaired compared to the C:50 species and those with higher carbon numbers. This effect was more marked in the male than in the female corpulent rats. The results indicate that VLDL hyperlipidemia in the corpulent rat is due to hepatic hypersecretion of VLDL and not to a defect in lipoprotein lipase. Further, the atherogenesis that is characteristic of the corpulent male rat may be related to the differential metabolism of fatty acids.
Arteriosclerosis
PMID:Plasma lipid secretion and clearance in hyperlipidemic JCR:LA-corpulent rats. 259 65

Rats of the atherosclerosis-prone JCR:LA-corpulent strain were subjected to long-term low (0.5% wt/vol) or high (4% wt/vol) consumption of ethanol from 1 to 12 months of age. The corpulent rats are hyperphagic, obese, and insulin-resistant; exhibit a marked very low density lipoprotein hyperlipidemia; and develop both vascular and myocardial lesions while eating a normal rat chow. The total lipid profile of the rat sera showed only limited changes with ethanol consumption. There were also no significant effects on high density lipoprotein lipids. Ethanol consumption was associated with elevated fasting glucose concentrations in both lean and corpulent rats and a strong decrease in fasting insulin levels and pancreatic B-cell volume density in the hyperinsulinemic corpulent rats. The relative frequency of myocardial nodules of chronic inflammatory cells was increased in the ethanol-consuming rats, both lean and corpulent. In contrast, old organized lesions (scars) were absent in the ethanol-consuming corpulent rats. Thus, ethanol consumption had no major effect on serum lipids or lipoproteins in the corpulent rat but was associated with a reduction in insulin resistance and islet cell hyperplasia, with an associated decreased incidence of myocardial lesions.
Arteriosclerosis
PMID:Effects of chronic ethanol consumption in atherosclerosis-prone JCR:LA-corpulent rat. 264 22

Diabetes mellitus is the most frequent endogenous cause of fat metabolism-disorder. In diabetics the risk for arteriosclerosis is significantly higher and the clinical significance of hyperlipidemia should be estimated more serious as in non-diabetics. The predominant abnormality of fat metabolism in diabetes is hypertriglyceridemia due to an increase of triglyceride-carrying lipoproteins, the chylomicrons and the very-low-density lipoproteins. In type I-diabetics the decisive pathogenetic factor for hypertriglyceridemia is the impaired degradation of VLDL and the reduced chylomicron-clearance, caused by decreased activity of the lipoproteinlipase. In ketoacidosis there is an additional increase in hepatic VLDL-triglyceride-production due to increased lipolysis with elevated free-fatty-acid flux. Total cholesterol in type I-diabetics is only significantly elevated when metabolic control is poor, low-density lipoprotein (LDL-)-cholesterol-levels can be increased and high-density lipoprotein (HDL-)cholesterol decreased in dependence on the metabolic control. In type II-diabetics the decisive pathogenetic factor for hypertriglyceridemia is increased VLDL-triglyceride-synthesis in the liver especially due to augmented free-fatty-acid flux. Additionally the activity of the lipoproteinlipase can be reduced. Usually in non-insulin-dependent diabetics LDL-cholesterol-levels can be seen elevated and HDL-cholesterol-concentration decreased in correlation with the metabolic control. Primary hyperlipoproteinemia appears frequently in diabetics, but this can be explained by the association with obesity in type II-diabetics.
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PMID:[Disorders of lipid metabolism in diabetes mellitus]. 269 31

Diabetes Mellitus represents an important public health problem in the most developed industrialized countries. Clinical presentations of diabetes are strongly related to the cardiovascular system, namely, coronary disease and angiopathic renal failure. Diabetes modifies the clinical course of arteriosclerosis by carrying the angiopathic process to a microvascular level, where typical microangiopathic lesions can be observed. The risk of developing atherosclerotic disease is 2-3 fold higher in diabetics than in nondiabetics and arterial hypertension reaches a prevalence of 40 to 80%. Authors analyse Arterial Hypertension in the context of Diabetes putting focus on the underlying pathophysiological mechanisms. Where considering the coronary disease (CD), its high prevalence among the diabetics is also emphasized, which is expressed by an increase of morbidity and mortality when compared to normal subjects. In diabetics not only the incidence of Acute Myocardial Infarction is higher, but also the long term prognosis is more complicated, a reality that the authors try to explain by anatomic and metabolic factors. The association of Diabetes plus hyperlipidemia represents undoubtedly one of the major factors that justify the worsening and progression of CD. Briefly, some interesting points that allow the understanding of this topic are described, pointing the pathogenic differences of types I and II and the clinical implications of their knowledge. Finally, the approach of Diabetes as a cardiovascular risk factor is discussed in a prophylactic perspective.
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PMID:[Diabetes mellitus and coronopathy]. 269 90


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