Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the association of in vivo concentrations of insulin, obesity, and gender with lipoprotein(a) [Lp(a)] levels, we used a cross-sectional population-based survey of a multistage random sample of the Mexico City adult population. We studied 423 normoglycemic, normotensive subjects from an original sample of 825, comprised of 239 men and 189 women with a mean age of 38.6 years (range, 17 to 90). All subjects were divided into 8 groups according to body mass index, fasting insulin, and gender. Lp(a) concentrations (mg/dL) were similar in obese women with and without high insulin levels (19.9 v 18.6), but hyperinsulinemic obese men had significantly lower Lp(a) levels than normoinsulinemic obese men (7.9 v 29.4). In addition, the proportion of obese men with Lp(a) concentrations of > or = 30 mg/dL was significantly higher in the normoinsulinemic than in the hyperinsulinemic (29.2% v 0.0%). The frequency distribution of Lp(a) levels was shifted to a lower range in hyperinsulinemic men compared with normoinsulinemic men. Our results show that in men, hyperinsulinemic obesity is associated with low Lp(a) levels, while obesity with normoinsulinemia is related to increased Lp(a) concentration. These observations were not found in women. These findings may explain the conflicting results reported by several studies.
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PMID:Differential effects of obesity with and without hyperinsulinemia on plasma lipoprotein(a) concentrations in men. 1122 26

Obesity is commonly cited as a risk factor for the development of coronary heart disease (CHD). Epidemiologic studies tend to support this contention, particularly those focusing on patients with central obesity. Such studies however, are imprecise and prone to misclassification bias. Angiographic and post mortem studies have demonstrated little or no correlation of total fat mass and coronary atherosclerosis except in those with abdominal obesity. There is a strong association of obesity, particularly central obesity, and traditional risk factors for CHD such as hypertension, type II diabetes mellitus, and dyslipidemia. There may also be an association between obesity and several nontraditional risk factors such as hyperhomocystinemia, elevated Lp(a) levels and factors that increase thrombogenesis. Obesity may also alter endothelial function. Weight loss, although associated with favorable modification of multiple risk factors for CHD, has not been shown to independently and definitively reduce CHD risk.
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PMID:Obesity and coronary heart disease. 1130 63

Peroxisome proliferation-activated receptor-gamma2 (PPARgamma2) is exclusively expressed in adipose tissue and belongs to the transcriptional regulators of adipocyte differentiation. Recently, two missense single-point mutations have been described in the PPARgamma2 gene: Pro12Ala and Pro115Gln. It was our aim to determine the frequency of these polymorphisms in a Caucasian cohort and to investigate their possible role in the pathogenesis of obesity, type 2 diabetes, and related metabolic disorders. The genotypes of 359 subjects (149 males, 210 females) with varying degrees of obesity and with or without type 2 diabetes were determined. Subsequent to genomic polymerase chain reaction amplification, the HpaII restriction fragment length polymorphism (RFLP) analysis and the HindII RFLP analysis were used for genotyping the Pro12Ala and Pro115Gln polymorphism, respectively. For the Pro115Gln polymorphism, all 359 subjects showed wild-type sequence, emphasizing the very rare occurrence of the mutated allele. For the Pro12Ala polymorphism, 276 subjects (76.9%) were homozygous for the wild-type allele, 80 (22.3%) were heterozygous, and only 3 (0.8%) were homozygous for the mutated allele. Genotype frequency was calculated to be 0.88 for the wild-type allele and 0.012 for the mutated allele. No significant differences were found in age; gender; body mass index; total cholesterol; low-density, high-density, and very low density lipoproteins; triglycerides; Lp(a); uric acid; and diabetes manifestation by comparing the different genotypes. Therefore, a major role of these polymorphisms in the pathogenesis of obesity and diabetes can be excluded.
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PMID:Frequency and significance of Pro12Ala and Pro115Gln polymorphism in gene for peroxisome proliferation-activated receptor-gamma regarding metabolic parameters in a Caucasian cohort. 1144 35

Cardiovascular disease (CVD) is the main cause of death. Atherosclerosis of coronary arteries is responsible for almost all cases of CVD. The term 'risk factor' describes all those characteristics found in healthy individuals that are independently related to subsequent development of CVD. It includes modifiable biochemical and physiological characteristics, such as hypercholesterolaemia, hypertension, cigarette smoking, diabetes mellitus, obesity and low HDL cholesterol levels, as well as non-modifiable personal characteristics, such as age, gender and family or personal history of early onset CVD. In addition to the 'classic' risk factors mentioned above, several other variables have been implicated as predictors of CVD: left ventricular hypertrophy; infectious agents; markers of inflammation; oxidative stress; and increased levels of fibrinogen, triglycerides, homocysteine and Lp(a)]. However, controversy exists regarding the exact role of these variables in the pathogenesis of atherosclerosis. Furthermore, there are no conclusive data showing that the modification of these variables is associated with a decrease in the incidence of cardiovascular events. Nevertheless, these 'new' risk factors should be taken into account in patients with CVD without established risk factors.
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PMID:The treatment of coronary heart disease: an update. Part 1: An overview of the risk factors for cardiovascular disease. 1146 41

The prognosis of patients suffering from severe hyperlipidemia, sometimes combined with elevated lipoprotein (a) (Lp[a]) levels, and coronary heart disease (CHD) refractory to diet and lipid-lowering drugs is poor. For such patients, regular treatment with low-density lipoprotein (LDL) apheresis is the therapeutic option. Today, there are four different LDL-apheresis systems available: immunoadsorption, heparin-induced extracorporeal LDL/fibrinogen precipitation, dextran sulfate LDL-adsorption, and LDL-hemoperfusion. Despite substantial progress in diagnostics, drug therapy, and cardiosurgical procedures, atherosclerosis with myocardial infarction, stroke, and peripheral cellular disease still maintains its position at the top of morbidity and mortality statistics in industrialized nations. Established risk factors widely accepted are smoking, arterial hypertension, diabetes mellitus, and central obesity. Furthermore, there is a strong correlation between hyperlipidemia and atherosclerosis. Besides the elimination of other risk factors, in severe hyperlipidemia (HLP) therapeutic strategies should focus on a drastic reduction of serum lipoproteins. Despite maximum conventional therapy with a combination of different kinds of lipid-lowering drugs, however, sometimes the goal of therapy cannot be reached. Mostly, the prognosis of patients suffering from severe HLP, sometimes combined with elevated Lp(a) levels and CHD refractory to diet and lipid-lowering drugs is poor. Hence, in such patients, treatment with LDL-apheresis can be useful. Regarding the different LDL-apheresis systems used, there were no significant differences with respect to the clinical outcome or concerning total cholesterol, LDL, high-density lipoprotein, or triglyceride concentrations. With respect to elevated Lp(a) levels, however, the immunoadsorption method seems to be the most effective. The published data clearly demonstrate that treatment with LDL-apheresis in patients suffering from severe hyperlipidemia refractory to maximum conservative therapy is effective and safe in long-term application.
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PMID:Current topics on low-density lipoprotein apheresis. 1172 15

Obesity is very frequently found after renal transplantation (Tx). It may represent risk factor for development of atherosclerosis and chronic allograft nephropathy. In a prospective randomized metabolic study we monitored for a period of 12 months a total of 427 patients (pts) (M 228/F 199) aged 20-70 yrs after Tx. All patients were treated with cyclosporin A and prednisone at standard doses. We compared the findings of 118 pts with a body mass index (BMI) > or = 30 (kg/m2, Group I) with data obtained from 309 pts with BMI < 30 (Group II) one year after Tx. The mean values of the analysed parameters were as follows (Gr I vs Gr II): total cholesterol (TC): 7.2 +/- 2.4 vs 6.1 +/- 2.0, triglycerides (TG) 3.8 +/- 1.6 vs 2.6 +/- 0.6; LDL-cholesterol 4.1 +/- 1.2 vs 3.0 +/- 0.7; fasting glycemia 8.0 +/- 3.2 vs 5.2 +/- 2.0 (all mmol/L, all p < 0.01); HDL-cholesterol/TG 0.28 +/- 0.07 vs 0.38 + 0.06, p < 0.025). The mean values of corrected Ccr, cyclosporine level, Lp(a) and proteinuria did not differ significantly. There were also no statistical differences in apo E isoforms. In conclusion, our data suggest hyperlipidemia-associated obesity should be treated effectively as a high-risk factor after Tx.
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PMID:Hyperlipidemia and obesity after renal transplantation. 1180 13

Hypoandrogenemia in men and hyperandrogenemia in women are associated with increased risk of coronary artery disease but also with visceral obesity, insulin resistance, low high-density lipoprotein (HDL) cholesterol, elevated triglycerides, low-density lipoprotein (LDL) cholesterol and plasminogen activator inhibitor (PAI-1). These gender differences and confounders render the precise role of endogenous androgens in atherosclerosis unclear. Exogenous androgens, on the other hand, induce both apparently beneficial and deleterious effects on cardiovascular risk factors by decreasing serum levels of HDL-C, PAI-1 (apparently deleterious), Lp(a), fibrinogen, insulin, leptin and visceral fat mass (apparently beneficial) in men as well as women. However, androgen-induced declines in circulating HDL-C should not automatically be assumed to be pro-atherogenic, since it may reflect accelerated reverse cholesterol transport instead.Short-term application of supraphysiological doses of exogenous T can reduce the severity and frequency of angina pectoris and improve the electrocardiographic signs of myocardial ischaemia; long-term effects have not been investigated. Nonetheless, interpretations of the effects of pharmacological doses of androgens on arterial compliance and flow-mediated dilatation in particular must be treated with circumspection also because at physiological concentrations, beneficial, neutral, and detrimental effects on vascular reactivity can be observed.Testosterone exerts 'pro-atherogenic' effects on macrophage function by facilitating the uptake of modified lipoproteins and an 'anti-atherogenic' effect by stimulating efflux of cellular cholesterol to HDL. In the majority of animal experiments, exogenous testosterone exerted neutral or beneficial effects on the development of atherosclerosis. In conclusion, the overall effect of administration of testosterone on cardiovascular-disease risk is difficult to assess because androgens have such an extraordinary array of effects in vivo. When dealing with a complex multifactorial condition such as CAD, it is premature to assume that clinical benefits can be derived from manipulation of the sex steroid milieu - even when these assumptions are based on biologically plausible mechanisms or, indeed, on cross-sectional risk-factor observational data. Neither needs the therapeutic use of testosterone in men be restricted by concerns regarding cardiovascular side effects.
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PMID:Testosterone and atherosclerosis. 1291 31

Lipoprotein(a) (Lp(a)) is regarded as an independent risk factor for Atherosclerotic cardiovascular disease. The objectives of this study were: to determine the effects of diet and exercise on Lp(a) and to evaluate the relation of Lp(a) with the lipid profile (total serum cholesterol (TC), triglycerides (TG), low density lipoprotein (LDL) and high density lipoprotein (HDL) cholesterol). Baseline Lp(a), body mass index (BMI) and the lipid profiles were measured in 343 Obese (BMI >30kg/m(2)) African-Americans. After a 3-month intervention of diet and exercise by 105 participants, their lipids were re-measured. Baseline Lp(a) levels ranged from 1.2 to 280mg/dl. Lp(a) was inversely associated with triglyceride (P<0.05). After the intervention, Lp(a) and HDL increased by a mean of 20 and 5%, respectively. Total cholesterol, triglycerides, LDL and BMI decreased by 7, 10, 11 and 8%, respectively. Women taking estrogen replacement had a negligible change in Lp(a) while participants taking HMG-CoA reductase inhibitors had an increase in Lp(a) levels by 30%.
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PMID:Response of lipoprotein(a) levels to therapeutic life-style change in obese African-Americans. 1470 70

The lipoprotein(a) [Lp(a)] and apolipoprotein E (apoE) polymorphisms have been shown to be important genetic determinants of cardiovascular risk. Their effect on coronary heart disease (CHD) is less clear, particularly in Asian Indians who are at high risk for this disease. The aim of this study was to examine the association of the Lp(a) promoter pentanucleotide repeat polymorphism and the apoE codon 112 and 158 genotypes in 195 young South African Indian patients (< or = 45 years) with myocardial infarction (MI). Results were compared with 300 healthy age-matched control subjects drawn from the same community and 107 unaffected siblings (18-45 years). In addition, fasting lipograms were performed on all patients and a detailed history of conventional risk factors and family background was obtained. Of the six different Lp(a) alleles detected, the 8-repeat sequence was most frequently seen. However, no difference in frequencies existed between patient and control groups. The most frequently occurring apoE genotype in the three study groups was E3/E3 (patients 71%; siblings 70%; controls 70%). A significant difference in the E3/E4 genotype was seen between patients and controls (23% vs 14%; p = 0.018) and between siblings and controls (24% vs 14%; p = 0.027). These patients were also more likely to have significantly higher low-density lipoprotein (LDL) and lower high-density lipoprotein (HDL) levels (p = 0.005 and 0.045, respectively). No association was observed between any of the Lp(a) or apoE genotypes and conventional risk factors such as smoking, diabetes, hypertension, obesity or a family history of CHD. In conclusion, the apoE3/E4 genotype is strongly associated with the incidence of myocardial infarction in young South African Indians. This genotype also adversely affects LDL and HDL cholesterol levels, both of which contribute to premature atherosclerosis. In contrast, the Lp(a) pentanucleotide repeat polymorphism does not appear to have any aetiological role in MI in this population.
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PMID:Lp(a) and apoE polymorphisms in young South African Indians with myocardial infarction. 1525 20

From 1998 to 2003, 133 Caucasian women aged 17-40 years (median 29 years) suffering from unexplained recurrent miscarriage (uRM) were consecutively enrolled. In patients and 133 age-matched healthy controls prothrombotic risk factors (factor V (FV) G1691A, factor II (FII) G20210A, MTHFR T677T, 4G/5G plasminogen activator inhibitor (PAI)-1, lipoprotein (Lp) (a), protein C (PC), protein S (PS), antithrombin (AT), antiphospholipid/anticardiolipin (APA/ACA) antibodies) as well as associated environmental conditions (smoking and obesity) were investigated. 70 (52.6%) of the patients had at least one prothrombotic risk factor compared with 26 control women (19.5%; p<0.0001). Body mass index (BMI; p=0.78) and smoking habits (p=0.44) did not differ significantly between the groups investigated. Upon univariate analysis the heterozygous FV mutation, Lp(a) > 30 mg/dL, increased APA/ACA and BMI > 25 kg/m(2) in combination with a prothrombotic risk factor were found to be significantly associated with uRM. In multivariate analysis, increased Lp(a) (odds ratio (OR): 4.7/95% confidence interval (CI): 2.0-10.7), the FV mutation (OR:3.8/CI:1.4-10.7), and increased APA/ACA (OR: 4.5/CI: 1.1-17.7) had independent associations with uRM.
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PMID:Lipoprotein (a) and other prothrombotic risk factors in Caucasian women with unexplained recurrent miscarriage. Results of a multicentre case-control study. 1588 1


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