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)

Beta-carotene in doses of up to 300 mg daily raises high-density lipoprotein cholesterol levels within 2 to 4 weeks in healthy subjects. The authors, in this study, investigate the short-term effects of high-dose beta-carotene upon serum lipids, lipoproteins, and selected sex steroid hormones in 59 adult patients with Type IIa or IIb hyperlipidemia and 36 healthy subjects. Volunteers took beta-carotene (300 mg) or wheat germ oil capsules daily for 30 days. Lipids were measured on days 1, 14, 21, and 30. Beta-carotene, retinol, free and total testosterone, and estradiol levels were measured on days 1 and 30. Total high-density lipoprotein cholesterol levels increased 10% (p < 0.01) over baseline in all groups by day 14 but returned to baseline by day 30. Total cholesterol, low-density lipoprotein cholesterol, and triglyceride levels transiently increased between days 14 and 21 by up to 9%, 8%, and 20%, respectively, only in the patients with hyperlipidemia treated with beta-carotene, but returned to baseline on day 30. Apolipoproteins A and B were unchanged. Despite 20-fold increases of plasma beta-carotene levels there, were no reports of carotenodermia and no alteration in sex steroid hormones, retinol levels, hepatic transaminases, or persistent changes in serum lipids that were attributable to beta-carotene.
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PMID:Lack of effects of beta-carotene on lipids and sex steroid hormones in hyperlipidemics. 801 Mar 32

A 59-year-old patient suffering from hyperlipidaemia developed a chronic vitamin A intoxication syndrome after ingestion of 30000 IE retinol/daily over a period of six years. Functional disability of the right hip was caused by radiologically documented hyperostosis of the acetabular circumference. Finally, a prosthesis had to be implanted because of rapid destructive osteoarthritis of the right hip. Implications of vitamin A for rheumatological management are discussed.
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PMID:Reduced vitamin A tolerance in a hyperlipidaemia patient with rapid destructive and hyperostotic osteoarthritis of the hip. 808 77

After the ingestion of a fat-rich meal, there is a postprandial increase in the plasma concentration of both apolipoprotein B-48- and apoB-100-containing triglyceride-rich lipoproteins (apoB-48 and apoB-100 TRL). In order to determine the contribution of these lipoproteins to postprandial lipemia, the concentration of triglycerides (TG) and retinyl esters (RE) was measured in apoB-48 and apoB-100 TRL after an oral fat load. Six normolipidemic male subjects were fed heavy cream (1 g fat per kg body weight) containing vitamin A (3000 retinol equivalents). TRL were isolated by ultracentrifugation from plasma samples obtained at regular intervals after the meal, and apoB-100 TRL were separated from apoB-48 TRL by affinity chromatography using monoclonal antibodies. Postprandial increase in plasma TG concentration was due to an increase in TG in the TRL fraction, which in turn was predominantly (82 +/- 4%) due to an increase in TG in apoB-48 TRL. Contribution of apoB-100 TRL to postprandial increase in TRL TG was 3-27% in individual subjects. ApoB-100 TRL remained a significant carrier of total plasma triglyceride in the fed state, as reflected by similar apoB-100 and apoB-48 TRL TG concentrations at 2, 4, and 6 h after the fat meal. Retinyl esters were regularly detected in apoB-100 TRL. Seventy-five (+/- 9) percent of the increase in TRL-RE was due to RE in apoB-48 TRL and 25 +/- 9% was due to RE in apoB-100. These data suggest that RE in plasma are not always associated with apoB-48-containing lipoproteins.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contribution of apoB-48 and apoB-100 triglyceride-rich lipoproteins (TRL) to postprandial increases in the plasma concentration of TRL triglycerides and retinyl esters. 830 Dec 24

The effect of dietary composition on concentrations of postprandial lipoproteins was studied in eight sulfonylurea-treated patients with noninsulin dependent diabetes mellitus. Two diets were consumed by each patient for 2 weeks in random order, one contained (as percent of total calories) 15% protein, 40% fat, and 45% carbohydrate (CHO), whereas the other consisted of 15% protein, 25% fat, and 60% CHO. At the end of each dietary period, patients were given Vitamin A (60,000 U/m2) with their noon meal, and the concentration of triglyceride (TG) and retinyl esters in plasma and two lipoprotein fractions (Sf > 400 and Sf 20-400) determined over the next 12 h. The results indicated that both postprandial TG and retinyl ester concentrations were higher in plasma (Sf > 400, and Sf 20-400 lipoproteins), when patients ate the 25% fat/60% CHO diet. Thus, replacing saturated fat with CHO accentuates the magnitude of postprandial lipemia. Since TG-rich lipoproteins may be atherogenic, appropriate dietary advice for patients with type 2 diabetes may deserve reappraisal.
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PMID:Effect of variations in dietary fat and carbohydrate intake on postprandial lipemia in patients with noninsulin dependent diabetes mellitus. 843 77

Vitamin A and its analogues have been reported to increase the release of tissue plasminogen activator in vitro. The aim of the present study was to reevaluate these findings and to investigate whether retinoids in doses used in dermatological therapy could enhance the release of endothelial fibrinolytic factors. Our results showed that endothelial cells incubated in vitro with retinoic acid increased the release of tissue plasminogen activator to the supernatant without concomitant secretion of plasminogen activator inhibitor-1. In patients treated with isotretinoin or etretinate these findings were confirmed, showing enhanced baseline tissue plasminogen activator concentrations in plasma in association with unchanged levels of plasminogen activator inhibitor-1 and von Willebrand factor. These findings are consistent with chronically augmented tissue plasminogen activator secretion without evidence of endothelial cell damage and may be of importance for the interpretation of the safety of lon-term therapy with regard to retinoid-induced hyperlipemia and the development of cardiovascular disease.
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PMID:Retinoids and fibrinolysis. 857 51

The authors present a case report of a 59-year-old female suffering from hyperlipidemia who developed chronic vitamin A intoxication syndrome after ingestion of 30,000 IU retinol/daily over a period of six years. The patient's main complaints included severe headaches, morning nausea, myalgias and disability around the hip, knee, and ankle joints. Radiologically, hyperostosis of the acetabular circumference and the spine was demonstrated. Because of rapidly increasing pain, total hip replacement was performed. Histology of cross sections from the femoral head revealed destructive osteoarthritis. Since no other causative reason was found, retinol may not only be responsible for hyperostotic bone and soft tissue formations but may perhaps also account for rapid progressing of degenerative joint disease. Despite the cessation of vitamin A intake the clinical symptoms persisted due to hyperlipidemia. The enlarged number of chylomicrons and the higher fraction of very low density lipoproteins may represent a second retinyl ester pool in case of overloaded fat storing Ito-cells in the liver. Therefore, rheumatological treatment reducing risk factors such as hyperlipidemia is mandatory.
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PMID:Hyperostotic and destructive osteoarthritis in a patient with vitamin A intoxication syndrome: a case report. 891 26

Orally ingested vitamin A (retinol) is incorporated into intestinal chylomicrons (CHYLO) in the form of retinyl esters (RE) along with newly absorbed dietary triglycerides (TG). As the intestinal lipoproteins undergo hydrolysis in the circulation, the majority of the RE remain with the secreted intestinal particles and have been used as a marker for intestinally derived lipoproteins during the early phase of the postprandial state. A multicompartmental model was developed for the kinetics of RE during postprandial lipemia in individuals with normal lipid levels (n = 16) and in patients with hyperlipidemia (n = 44). The assumptions used in the development of the model are presented in this report. Some of the key findings include (1) as much as 50% of the newly synthesized RE may be secreted by the intestine as very-low-density lipoprotein (VLDL)-sized particles of S(f) 20 to 400 following consumption of a test meal containing a moderate amount of fat (20 to 30 g); (2) in most individuals, approximately 50% of the RE secreted in S(f) greater than 400 are converted to smaller, less buoyant fractions, and 50% are irreversibly removed directly from the plasma; (3) as much as 5% to 20% of the ingested retinol may be secreted as small intestinal lipoproteins with the buoyance of low-density lipoprotein (LDL) in some individuals; and (4) less than 5% of RE flux through S(f) 20 to 400 is converted to S(f) less than 20, and the primary catabolic pathway for RE in this fraction is direct uptake. Comparable estimates can be obtained for the kinetic parameters when repeat studies are made in the same subjects under comparable conditions.
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PMID:Kinetics of retinyl esters during postprandial lipemia in man: a compartmental model. 916 Aug 28

There are indications that beta-carotene, but not pre-formed vitamin A, is protective on the risk of acute myocardial infarction (AMI). The relationship between nonfatal AMI and the intake of beta-carotene and retinol was investigated in a case-control study conducted between 1983 and 1992 in northern Italy on 433 women with nonfatal AMI and 869 controls in hospital for acute, non-cardiovascular, non-neoplastic, non-digestive, non-hormone related conditions. Odds ratios (OR), with their 95% confidence intervals (CI), were computed by unconditional multiple logistic regression analysis, including terms for age, education, body mass index, smoking, alcohol and coffee drinking, menopausal status, hormone replacement therapy and history of diabetes, hypertension and hyperlipidemia. The risk of AMI was inversely related to beta-carotene intake, with an OR of 0.5 (95% CI: 0.3 to 0.8) for the highest quintile of intake compared to the lowest (chi2 trend = 10.53, p < 0.01). Retinol intake was not associated with AMI, with an OR of 0.9 (95% CI: 0.6 to 1.3) for the highest quintile of intake compared to the lowest. Analysis in separate strata of covariates indicated that the inverse association of beta-carotene intake with risk of AMI was appreciably stronger in younger, lean women with no history of diabetes or hypertension, and in current smokers. The results of this study indicate that the risk of nonfatal AMI in women is inversely related to intake of beta-carotene containing foods, but not foods containing retinol.
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PMID:Beta-carotene intake and risk of nonfatal acute myocardial infarction in women. 932 8

As many as 20% of the survivors of acute myocardial infarction present with the heritable form of hyperlipidemia, termed familial combined hyperlipidemia (FCHL). Some of the genes reported to be involved in this disorder, such as those for lipoprotein lipase (LPL) and apolipoprotein (apo) C-III, are controlled by a peroxisome proliferator-activated receptor (PPAR)/retinoic acid receptor X (RXR) regulatory system, which is retinoic acid dependent. If, as we hypothesized, the availability of retinoic acid or its precursor retinol (vitamin A) could be altered in FCHL, this could help explain some aspects of the phenotypic expression of the disease. We therefore measured plasma retinol concentrations in 30 FCHL subjects and 56 controls. Plasma retinol concentrations in FCHL subjects were significantly lower than that of control subjects (1.96 +/- 0.83 mumol/L vs 2.91 +/- 1.23 mumol/L, respectively; P < 0.0001). This novel finding of significantly decreased concentrations of plasma retinol in FCHL relative to control subjects gives support to the hypothesis that vitamin A might be involved in the expression of this disorder.
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PMID:Low plasma vitamin A concentrations in familial combined hyperlipidemia. 943 57

There is growing evidence of the capacity of vitamin A to regulate the expression of the genetic region that encodes apolipoproteins (apo) A-I, C-III, and A-IV. This region in turn has been proposed to modulate the expression of hyperlipidemia in the commonest genetic form of dyslipidemia, familial combined hyperlipidemia (FCHL). The hypothesis tested here was whether vitamin A (retinol), by controlling the expression of the AI-CIII-AIV gene cluster, plays a role in modulating the hyperlipidemic phenotype in FCHL. We approached the subject by studying three genetic variants of this region: a C1100-T transition in exon 3 of the apoC-III gene, a G3206-T transversion in exon 4 of the apoC-III gene, and a G-75-A substitution in the promoter region of the apoA-I gene. The association between plasma vitamin A concentrations and differences in the plasma concentrations of apolipoproteins A-I and C-III based on the different genotypes was assessed in 48 FCHL patients and 74 of their normolipidemic relatives. The results indicated that the subjects carrying genetic variants associated with increased concentrations of apoA-I and C-III (C1100-T and G-75-A) also presented increased plasma concentrations of vitamin A. This was only observed among the FCHL patients, which suggested that certain characteristics of these patients contributed to this association. The G3206-T was not associated with changes in either apolipoprotein concentrations or in vitamin A. In summary, we report a relationship between genetically determined elevations of proteins of the AI-CIII-AIV gene cluster and vitamin A in FCHL patients. More studies will be needed to confirm that vitamin A plays a role in FCHL which might also be important for its potential application to therapeutical approaches.
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PMID:Vitamin A is linked to the expression of the AI-CIII-AIV gene cluster in familial combined hyperlipidemia. 1006 30


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