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)

Short-term treatment of male and female obese JCR:LA-corpulent rats with beta,beta'-tetramethyl hexadecanedioic acid (MEDICA 16) resulted in a marked decrease (as much as 80%) in plasma triglyceride values, with a concomitant decrease in the highly elevated very low density lipoprotein (VLDL) levels of the corpulent rat. There were modest decreases in cholesterol levels and increases in low density lipoprotein and high density lipoprotein lipids. The concentrations of apolipoproteins C-II and C-III were decreased in both the whole-serum and the VLDL fractions. Food consumption, rate of weight gain, fasting insulin levels, and the integrated insulin response to an intravenous glucose load remained unaffected. The decrease in plasma VLDL may be accounted for by inhibition of liver long-chain fatty acid synthesis at the level of ATP citrate lyase, with a concomitant reduction of VLDL triglyceride production by the liver. This decrease in plasma VLDL production was accompanied by a twofold to threefold increase in the triglyceride and cholesterol components of the low density lipoprotein and high density lipoprotein fractions, together with a twofold to fourfold decrease in plasma apolipoprotein, indicating that activation of plasma VLDL catabolism may further account for the overall hypolipidemic effect induced by MEDICA 16. The overall hypolipidemic effect of MEDICA 16 may be expected to inhibit the spontaneous atherogenic sequelae induced in the corpulent rat by severe VLDL hyperlipidemia.
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PMID:Hypolipidemic effect of beta, beta'-tetramethyl hexadecanedioic acid (MEDICA 16) in hyperlipidemic JCR:LA-corpulent rats. 202

A 53-year old woman developed excessive hypertriglyceridemia (greater than 10,000 mg/dl) with features of toxic liver damage after prolonged ethanol ingestion. Lipoprotein-lipase-activity was not decreased, apolipoprotein-C-II analysis, as shown by gel-electrophoresis, revealed a regular pattern. Treatment with parenteral nutrition and abstinence of ethanol resulted in a complete normalization of plasma triglycerides after transient remnant-hyperlipidemia. Decrease of triglycerides was accompanied by declining liver enzyme activities. As suggested by unimpaired activity of lipolysis, the extent of hypertriglyceridemia may be explained by a reversible receptor mediated defect of hepatic catabolism, aggravated by hepatic overproduction of triglyceride-rich-particles. Although receptor dysfunction is not yet understood, the transient appearance of remnant particles may be a helpful criteria in diagnosis of ethanol induced hypertriglyceridemia.
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PMID:[Pathogenesis of alcohol-induced hyperlipidemia: case report of hypertriglyceridemia over 10,000 mg%]. 208 70

Assessment of the relative transcription rates and mRNA steady-state levels for apolipoprotein genes E, A-I, and A-II has been performed in normal rat liver, during liver regeneration and following induction of cirrhosis, as well as in rats with inherited analbuminemia associated with hyperlipidemia. Apo E exhibits primarily transcriptional control with an additional component of posttranscriptional control, whereas Apo A-I is controlled primarily at the posttranscriptional level, thus indicating that these genes are regulated independently. The level of control for Apo A-II has not been determined, because of difficulty experienced in measuring the transcription rate of this gene. During liver regeneration, cirrhosis, and analbuminemia, there is a marked increase in the ratio of Apo A-I to Apo E mRNA, resulting from an increase in the Apo A-I mRNA steady-state level and a decrease in Apo E mRNA. These changes are similar in the three pathophysiologic states and seem to occur through a combination of transcriptional and posttranscriptional mechanisms.
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PMID:Transcriptional and posttranscriptional regulation of apolipoprotein E, A-I, and A-II gene expression in normal rat liver and during several pathophysiologic states. 212 16

The study objective was to determine the effects of monotherapy with clonidine and atenolol versus placebo on serum lipids, apolipoproteins, and blood pressure in patients with mild primary hypertension. The protocol comprised a double blind, randomized, placebo-controlled 5-month prospective study carried out in an outpatient general internal medicine clinic in a university medical center. There were 92 patients ages 18 to 70, with mild primary hypertension (sitting diastolic blood pressure of greater than 90 mm Hg and less than 105 mm Hg) without significant cardiac, renal, cerebrovascular, hepatic, neoplastic, or hematologic disorders. Patients with severe hyperlipidemia or peripheral vascular disease were also excluded. All factors known to effect serum lipids were held constant throughout the study (i.e., diet, weight, exercise, caffeine, tobacco). Atenolol and clonidine significantly reduced blood pressure when compared with placebo. Atenolol caused significant increases in serum triglycerides and apolipoprotein B (p less than 0.05) and significant reductions in high-density lipoprotein-cholesterol, apolipoproteins A-I and A-II (p less than 0.05). Atenolol also induced a significant adverse effect on all lipid ratios, increasing total cholesterol/high density lipoprotein-cholesterol, low density lipoprotein-cholesterol/high density lipoprotein-cholesterol, apolipoprotein B/apolipoprotein A-I and apolipoprotein B/apolipoprotein A-II ratios and decreasing low density lipoprotein-cholesterol/apolipoprotein-B ratio (p less than 0.05). Clonidine caused significant reductions in high-density lipoprotein-cholesterol, apolipoproteins AI and AII (p less than 0.05 but was neutral on all other lipids, lipid subfractions, and apolipoproteins. Clonidine did not significantly alter any of the lipid ratios.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of clonidine hydrochloride versus atenolol monotherapy on serum lipids, lipid subfractions, and apolipoproteins in mild hypertension. 219 93

A causal link between hypercholesterolemia due to elevated plasma concentrations of LDL and VLDL remnants of CAPD patients has been established. The effects of 24 weeks of treatment with Simvastatin, a new HMG coenzyme A-reductase inhibitor (at 20 and 40 mg/day) on serum lipid, lipoprotein, and apolipoprotein A-I and B concentrations, as well as safety parameters and subjective side effects, were evaluated in eight patients (mean duration CAPD 24.80 +/- 7.50 months, age 54.50 +/- 13.70 years). Maximal effects on plasma lipoprotein and apolipoprotein concentrations were achieved after 4 weeks, and remained stable thereafter during the study. Mean fasting plasma cholesterol concentrations decreased from 280.5 +/- 60.2 mg% to 190.2 +/- 40.4 mg/dl (p less than 0.005) (-47%); mean plasma LDL-cholesterol concentrations also decreased from 257.6 +/- 13.4 mg% to 190.5 +/- 15.4 mg/dl (p less than 0.001) (-35%). Apolipoprotein A and B concentrations decreased significantly from 1.78 +/- 0.19 to 1.40 +/- 0.22 g/L (p less than .005) and 1.81 +/- 0.26 to 1.38 +/- 0.20 g/L (p less than .005). These data substantiate the view that Simvastatin is well tolerated and that no serious clinical or adverse laboratory effects have been observed. It appears to be a promising drug for the effective control of hyperlipemia in a large proportion of hypercholesterolemic patients, reducing their cardiovascular morbidity while on CAPD.
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PMID:Therapeutic effects of simvastatin on hyperlipidemia in CAPD patients. 225 55

A total of 51 cases with hyperlipidemia, who were defined deficiency symptom-complex complicated by symptoms of excessiveness in TCM were studied clinically. The patients were divided into two groups at random. One group was treated with Xiaobu Jianfei Pian (XJP) as treated group, another with Fangfeng Tongsheng San as a control. It was found that XJP was able to lower total serum cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and apolipoprotein (apo) B significantly (P less than 0.001, 0.001, 0.001) while it had markedly improved clinical symptoms. It was also observed that XJP had good effects on the ratios of apoA1/B and TC/HDL-C, and was able to reduce body weight index. All of these were better than those of the control group statistically. These evidences indicate that XJP possesses clinical therapeutic effects on both lipid-lowering and lipid-adjusting, which suggest that XJP may be an effective anti-hyperlipidemia medicine.
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PMID:[Hyperlipidemia treated with xiaobu jianfei pian]. 226 40

Atherosclerosis is the main cause of death in diabetes mellitus. This may at least in part be due to lipoprotein abnormalities which have been described in these patients. Apolipoprotein-E is a component of most lipoprotein fractions and plays an important role in the catabolism of VLDL. The different apolipoprotein-E phenotypes determined genetically are associated with certain hyperlipoproteinemias in a various degree in nondiabetic patients. In most cases apolipoprotein-E phenotype E2/2 is characteristic for familial dysbetalipoproteinemia. Phenotype E3/2 was found to be more frequent in hypertriglyceridemia while phenotype E4/3 was associated with hypercholesterolemia as well as with type V hyperlipoproteinemia. We studied apolipoprotein-E phenotypes and serum lipids in 141 type II diabetic patients (36 normolipidemic 41 type IIa hyperlipidemic, 32 type IIb hyperlipidemic, 24 type II hyperlipidemic, 8 type V hyperlipidemic). the phenotype E3/3 was more common in normolipidemic diabetic (77.8%) than in hyperlipoproteinemic diabetic patients (42.9%) or in the control group (57.5%). On the other hand phenotype E3/2 was more frequent in hypertriglyceridemic (50%) than in normolipidemic (5.6%) or hypercholesterolemic (hyperlipoproteinemia IIa: 4.9%, IIb: 9.4%) diabetic patients. The phenotype E4/3 was more frequent in all hyperlipoproteinemic diabetic patients, especially in those having hypercholesterolemia (34.2%) or mixed hyperlipidemia (50%). In conclusion we found a strong association between apo-E2 and hypertriglyceridemia in diabetic patients. This association was stronger than the one found in the general population. The association between apo-E4 and hypercholesterolemia in diabetic patients was similar to the one described in non-diabetic patients. We therefore conclude that type II diabetes mellitus is a possible cofactor in the apolipoprotein-E2 associated hyperlipoproteinemia.
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PMID:Apolipoprotein E phenotype frequency in type II diabetic patients with different forms of hyperlipoproteinemia. 227 5

The 127 diet-resistant primary hyperlipidemic patients received 100 mg of ciprofibrate daily for 12 weeks. In the 63 patients with type IIa hyperlipidemia and 41 patients with type IIb hyperlipidemia, serum levels of total cholesterol, very-low-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglycerides, very-low-density lipoprotein triglycerides, and apolipoprotein (apo) B decreased significantly and levels of high-density lipoprotein cholesterol and apo A-I increased significantly. Similar changes occurred in the 23 type IV patients, except that high-density lipoprotein cholesterol levels increased significantly and apo B levels did not change. No clinically significant side effects or drug-related abnormal laboratory test results were noted. It is concluded that ciprofibrate is a safe and potent hypolipidemic agent.
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PMID:Efficacy of ciprofibrate in primary type II and IV hyperlipidemia: the Italian multicenter study. 228 17

Hyperlipidemia is a consistent feature of the nephrotic syndrome. In this study, low-density lipoprotein (LDL) metabolism has been investigated in nine patients with nephrotic syndrome and varying degrees of proteinuria. In subjects with moderate proteinuria (less than 10 g/d), total plasma cholesterol values were elevated to approximately 160% of normal due mainly to an increase in circulating LDL cholesterol. Metabolic studies showed that a defect in LDL clearance via the receptor pathway was responsible for its accumulation. The total amount of LDL apolipoprotein catabolized by this mechanism was only 55% of the value seen in controls; 60% more LDL was channelled into alternative, receptor-independent, catabolic pathways. Heavier proteinuria was associated with substantial increases in plasma triglyceride and very-low-density lipoprotein (VLDL) levels. The defect in LDL catabolism was aggravated by oversynthesis of the lipoprotein, which expanded the plasma LDL pool to 250% of normal. These observations indicate that the hyperlipidemia of the nephrotic syndrome is multifactorial in origin. The altered catabolism of LDL may be important in predisposing these subjects to premature atherosclerosis.
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PMID:Low-density lipoprotein metabolism in the nephrotic syndrome. 229 90

Two patients with severe hyperlipidemia receiving long-term hemodialysis were classified as type III hyperlipoproteinemic subjects. They are homozygous for apolipoprotein E2 and have an elevated VLDL-cholesterol/plasma-triglyceride ratio. The dyslipoproteinemia was severely aggravated by the renal failure, but careful treatment with bezafibrate was able to effectively lower elevated serum lipids. Accurate diagnosis of lipid abnormalities in patients with chronic renal failure seems to be necessary to plan appropriate therapeutic interventions and to lower the risk for accelerated atherosclerosis.
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PMID:Severe type III hyperlipoproteinemia in two patients maintained on chronic hemodialysis. 231 34


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