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)

C-reactive protein (CRP) has been recognized as a useful marker for coronary or cardiovascular risk in healthy subjects or patients with coronary heart disease (CHD) in industrialized societies. We assessed whether CRP could serve as a marker of prevalent CHD risk in a cross-sectional study of a population with low cholesterol levels (4.61 mmol/L in men and 4.82 mmol/L in women) but higher prevalence of other risk factors. In 1,046 participants of the Turkish Adult Risk Factor Survey in 2000, high-sensitivity CRP as well as other risk variables were evaluated, and CHD was diagnosed, based on clinical findings and Minnesota coding of electrocardiograms at rest. Almost an equal number of men and women > or = 30 years of age constituted the population sample of the western regions of Turkey. Geometric mean value of CRP was 1.9 mg/L (interquartile range 0.8 to 4.3), without revealing a significant difference in gender. CRP was correlated with many variables, notably those involving central obesity, fibrinogen, and apolipoprotein-B, but not with smoking status (regardless of age adjustment). In multiple regression models, blood fibrinogen, waist circumference, total cholesterol, and physical activity grade were independently associated with log CRP concentrations. Among many risk variables, CRP quartiles and systolic blood pressure were, besides age and gender, the only significant independent determinants of CHD. The age-adjusted odds ratio for CHD in the highest as opposed to the lowest quartile was 4.48 (p < 0.001). Even after adjustment for the 5 previously mentioned determinants of CRP, a 4.2-fold increased risk of CHD still persisted between the highest and lowest quartiles. Thus, the observed increased risk was not in large part due to the intermediary effects of fibrinogen, nor were some indicators of insulin resistance, but interaction appeared to be independent of these effects. Thus, CRP values serve as a marker of prevalent CHD risk in populations with low cholesterol levels. This association is independent of, or in addition to, the effects of conventional risk factors, suggesting that the contribution of chronic low-grade inflammation to the atherothrombotic process is present even in the setting of low cholesterol levels.
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PMID:C-reactive protein and coronary heart disease in western Turkey. 1156 80

The corpulent JCR:LA-cp rat (cp/cp) is a useful model for study of the metabolic consequences of obesity and hyperinsulinemia. To assess the effect of hyperinsulinemia on VLDL secretion in this model, we measured rates of secretion of VLDL in perfused livers derived from cp/cp rats and their lean littermates. Livers of cp/cp rats secreted significantly greater amounts of VLDL triglyceride and apolipoprotein, compared with lean littermates. The content of apoB, apoE, and apoCs in both perfusate and plasma VLDL was greater in the cp/cp rat, as was the apolipoprotein (apo)C, apoA-I, and apoA-IV content of plasma HDL. Triglyceride content was also greater in cp/cp livers, as was hepatic lipogenesis and expression of lipogenic enzymes and sterol regulatory element binding protein-1 (SREBP-1). Hepatic mRNAs for apoE, and apoA-I were higher in livers of cp/cp rats. In contrast, the steady state levels of apoC-II, apoC-III, and apoB mRNAs were unchanged. Thus, livers of obese hyperinsulinemic cp/cp JCR:LA-cp rats secrete a greater number of VLDL particles that are enriched in triglyceride, apoE, and apoC. Greater secretion of VLDL in the cp/cp rat in part results from higher endogenous fatty acid synthesis, which in turn may occur in response to increased expression of the lipogenic enzyme regulator SREBP-1c.
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PMID:Increased hepatic VLDL secretion, lipogenesis, and SREBP-1 expression in the corpulent JCR:LA-cp rat. 1173 77

The effects of high-fat feeding on the development of obesity were evaluated in intercellular adhesion molecule-1 (ICAM-1) knockout and C57BL/6J (B6) male mice fed a high-fat diet for < or =50 days. Serum and tissues were collected at baseline and after 1, 11, and 50 days on the diet. After 11 days on the diet, ICAM-1-deficient, but not B6, mice developed fatty livers and showed a significant increase in inguinal fat pad weight. At day 50, ICAM-1-deficient mice weighed less, and their adiposity index and circulating leptin levels were significantly lower than those of B6 controls. To better understand the early differential response to the diet, liver gene expression was analyzed at three time points by use of Affymetrix GeneChips. In both strains, a similar pattern of gene expression was detected in response to the high-fat diet. However, sterol regulatory element-binding protein-1, apolipoprotein A4, and adipsin mRNAs were significantly induced in ICAM-1-deficient livers, suggesting that these genes and their associated pathways may be involved in the acute diet response observed in the knockout mice.
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PMID:Diet-induced obesity and hepatic gene expression alterations in C57BL/6J and ICAM-1-deficient mice. 1183 76

Current data suggest that phospholipid transfer protein (PLTP) has multiple metabolic functions, however, its physiological significance in humans remains to be clarified. To provide further insight into the role of PLTP in lipoprotein metabolism, plasma PLTP activity was measured, and lipoproteins were analyzed in 134 non-diabetic individuals on a controlled diet. Insulin sensitivity index (Si) and body fat composition were also determined. Plasma PLTP activity was comparable between men (n=56) and women (n=78). However, in women but not in men, plasma PLTP activity was positively correlated with cholesterol, triglyceride, low density lipoprotein (LDL) cholesterol, and apolipoprotein (apo) B (r=0.38-0.45, P< or =0.001), and with body mass index (BMI), subcutaneous and intra-abdominal fat (SCF, IAF) (r=0.27-0.29, P<0.02). Among the different apo B-containing lipoproteins (LpB) in women, PLTP was most highly correlated with intermediate density lipoproteins (IDL) and buoyant LDL (r=0.45-0.46, P<0.001). The correlation with IDL was significant only in women with BMI < or =27.5 kg/m(2) (n=56). In men with BMI < or =27.5 kg/m(2) (n=35), PLTP activity was significantly correlated with buoyant LDL (r=0.40, P<0.02) and high density lipoprotein (HDL) (r=0.43, P<0.01). These data provide evidence for a role of PLTP in LpB metabolism, particularly IDL and buoyant LDL. They also suggest that gender and obesity-related factors can modulate the impact of PLTP on LpB.
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PMID:Association of plasma phospholipid transfer protein activity with IDL and buoyant LDL: impact of gender and adiposity. 1200 24

Phospholipid transfer protein (PLTP) is a member of the lipid transfer/lipopolysaccharide binding protein gene family. Recently, the crystal structure of one of the members of the gene family, bactericidal permeability increasing protein, was solved, providing potential insights into the mechanisms of action of PLTP. These molecules contain intrinsic lipid binding sites and appear to act as carrier proteins that shuttle between lipoproteins to redistribute lipids. The phenotype of PLTP transgenic and gene knock out mice indicates that PLTP plays a major role in the metabolism of high-density lipoprotein (HDL) and apoB-containing lipoproteins and thereby influences the concentration, apolipoprotein content, and size of lipoprotein particles in plasma. Recent data indicate that PLTP deficiency in mice is associated with a decrease of atherosclerosis, despite decreased HDL levels. At lease two underlined mechanisms are involved in the reduction of atherosclerosis in PLTP deficient status, 1) reduction of apoB-containing lipoprotein production and levels; and 2) increase of anti-oxidation potential. Human studies indicated that PLTP activity positively correlated with aging, obesity, diabetes and coronary artery disease. A challenge for the future will be the inhibition of PLTP for therapeutic benefit.
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PMID:The effect of phospholipid transfer protein on lipoprotein metabolism and atherosclerosis. 1208 20

Altered plasma levels of lipids and lipoproteins, obesity, hypertension, and diabetes are major risk factors for atherosclerotic cardiovascular disease. To identify genes that affect these traits and disorders, we looked for association between markers in candidate genes (apolipoprotein AII (apo AII), apolipoprotein AI-CIII-AIV gene cluster (apo AI-CIII-AIV), apolipoprotein E (apo E), cholesteryl ester transfer protein (CETP), cholesterol 7alpha-hydroxylase (CYP7a), hepatic lipase (HL), and microsomal triglyceride transfer protein (MTP)) and known risk factors (triglycerides (Tg), total cholesterol (TC), apolipoprotein AI (apo AI), apolipoprotein AII (apo AII), apolipoprotein B (apo B), body mass index (BMI), blood pressure (BP), leptin, and fasting blood sugar (FBS) levels.) A total of 1,102 individuals from the Pacific island of Kosrae were genotyped for the following markers: Apo AII/MspI, Apo CIII/SstI, Apo AI/XmnI, Apo E/HhaI, CETP/TaqIB, CYP7a/BsaI, HL/DraI, and MTP/HhpI. After testing for population stratification, family-based association analysis was carried out. Novel associations found were: 1) the apo AII/MspI with apo AI and BP levels, 2) the CYP7a/BsaI with apo AI and BMI levels. We also confirmed the following associations: 1) the apo AII/MspI with Tg level; 2) the apo CIII/SstI with Tg, TC, and apo B levels; 3) the Apo E/HhaI E2, E3, and E4 alleles with TC, apo AI, and apo B levels; and 4) the CETP/TaqIB with apo AI level. We further confirmed the connection between the apo AII gene and Tg level by a nonparametric linkage analysis. We therefore conclude that many of these candidate genes may play a significant role in susceptibility to heart disease.
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PMID:Candidate genes involved in cardiovascular risk factors by a family-based association study on the island of Kosrae, Federated States of Micronesia. 1211 31

A total of 5 randomized, double-blind trials in patients with hypercholesterolemia were prospectively designed to allow pooling of plasma lipid data after 12 weeks of treatment. The purpose was (1) to compare rosuvastatin 5 and 10 mg with atorvastatin 10 mg (data from 3 of the 5 trials); (2) to compare rosuvastatin 5 and 10 mg with simvastatin 20 mg and pravastatin 20 mg (data from 2 of the 5 trials); and (3) to summarize overall efficacy and subset analyses of rosuvastatin data from all 5 trials. Rosuvastatin 5 mg (n = 390) and 10 mg (n = 389) reduced low-density lipoprotein (LDL) cholesterol significantly more than did atorvastatin 10 mg (n = 393) (41.9% and 46.7% vs 36.4%, both p <0.001). Treatment with rosuvastatin 5 mg (n = 240) and 10 mg (n = 226) also resulted in significantly greater reductions in LDL cholesterol compared with both simvastatin 20 mg (n = 249) and pravastatin 20 mg (n = 252) (40.6% and 48.1% vs 27.1% and 35.7%, all p <0.001). Significant differences favoring rosuvastatin 10 mg were also observed for total cholesterol, high-density lipoprotein (HDL) cholesterol, non-HDL cholesterol, apolipoprotein (apo) B, and apo A-I versus atorvastatin 10 mg, and for total cholesterol, HDL cholesterol, triglycerides, non-HDL cholesterol, and apo B versus simvastatin 20 mg and pravastatin 20 mg. Analyses of all the rosuvastatin 10 mg data (n = 615) from the 5 trials in subgroups defined by age > or =65 years, female sex, postmenopausal status, hypertension, atherosclerosis, type 2 diabetes, and obesity showed that rosuvastatin had consistent efficacy across patient subgroups.
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PMID:Efficacy of rosuvastatin compared with other statins at selected starting doses in hypercholesterolemic patients and in special population groups. 1264 36

The dysmetabolic syndrome of insulin resistance and visceral obesity is characterized by elevated plasma concentration of triacylglycerol-rich lipoprotein (TRL) remnants that may be related to increased cardiovascular risk. Perturbed hepato-intestinal cholesterol metabolism may play a contributory role in this abnormality. We therefore investigated the association between plasma markers of cholesterol absorption and synthesis with TRL remnant metabolism in 35 men with the metabolic syndrome (MS). Plasma campesterol:cholesterol and lathosterol:cholesterol ratios were measured as estimates of cholesterol absorption and synthesis respectively. Remnant metabolism was assessed by measuring remnant-like particle-cholesterol (RLP-C), apolipoprotein (apo)B-48 and the fractional catabolic rate (FCR) of a labelled remnant-like emulsion. Compared with controls, subjects with the MS had significantly lower plasma campesterol:cholesterol ratio, but higher lathosterol:cholesterol ratio ( P <0.05). Plasma RLP-C and apoB-48 concentrations were also higher ( P <0.01) and the remnant-like emulsion FCR was lower ( P <0.05). The plasma campesterol:cholesterol ratio was inversely correlated ( P <0.05) with plasma triacylglycerols ( r =-0.346), RLP-C ( r =-0.443), apoB-48 ( r =-0.427) and plasma lathosterol:cholesterol ratio ( r =-0.366); the campesterol:cholesterol ratio was also positively correlated with the remnant-like emulsion FCR ( r =0.398, P <0.05). In multiple regression analysis, the significant correlations between plasma campesterol:cholesterol ratio and plasma triacylglycerols, RLP-C, apoB-48 and FCR of the remnant-like emulsion were independent of age, dietary energy and plasma lathosterol. Our findings suggest that in subjects with the MS alterations in cholesterol absorption and synthesis may be closely linked with the kinetic defects in TRL metabolism.
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PMID:Relationships between cholesterol homoeostasis and triacylglycerol-rich lipoprotein remnant metabolism in the metabolic syndrome. 1265 82

To investigate the disorder of lipid metabolism and explore the possible mechanism of increasing risk of atherosclerosis(AS) in simple childhood obesity, serum lipids and apolipoprotein were examined. 49 obese children were selected and another 49 non-obese children were selected as control. Their serum lipids (TG, TC, VLDL-ch, HDL-ch and LDL-ch) and apolipoprotein(apoA1 and apoB100) were measured. The results showed TG, VLDL-ch, apoB100, artherosclerosis index (AI) and LDL-ch/HDL-ch ratio in childhood obesity were significantly higher than that in normal children (P < 0.05), while HDL-ch, apoA1, HDL-ch/TC, apoA1/apoB100 ratio in obese children were obviously lower than that in normal ones(P < 0.05). The results suggested that metabolic disorder of lipid and apolipoprotein took place in obese children. The disorder which may increase the risk of AS should be paid great attention.
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PMID:[Study on plasma lipids, apolipoprotein A1, apolipoprotein B100 in simple obese children]. 1272 89

Genetic variation in the microsomal triglyceride transfer protein (MTP) affects the secretion pattern and plasma concentration of apolipoprotein (aopB)-containing lipoproteins and a common functional -493 G/T polymorphism has been reported to influence plasma lipids levels. Recent data suggest that carriers of the T allele might be more sensitive to detrimental factors such as features of the insulin resistance syndrome. Since type 2 diabetes is associated with obesity and insulin resistance, the present study investigated the effect of this polymorphism on plasma lipids, apoB and LDL subfractions in 281 Chinese type 2 diabetic subjects and 364 non-diabetic controls. The frequency of the rare T allele was 0.162 and 0.126 in subjects with and without diabetes respectively. There were no differences in the effect of the polymorphism on plasma lipids and apoB in the two groups. However, the TT genotype was associated with a higher concentration of small dense LDL-III than the GT or GG variants in the diabetic subjects (P=0.01) whereas no such effect was observed in the controls. In the diabetic patients, age, plasma triglyceride and the MTP genotype were independent determinants of LDL-III concentrations in linear regression analysis (R(2)=10%, P=0.04) whereas in the controls, only plasma triglyceride and age were important determinants (R(2)=15%, P=0.01). In conclusion, the -493 G/T polymorphism only has a minor effect on LDL subfraction pattern in Chinese and the effect is only apparent in the presence of type 2 diabetes.
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PMID:Effect of the microsomal triglyceride transfer protein -493 G/T polymorphism and type 2 diabetes mellitus on LDL subfractions. 1281 11


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