UMLS:C0028754 - FACTA Search

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Query: UMLS:C0028754 (obesity)
124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present study was to examine the effect of variation at the apolipoprotein (apo) A-II gene locus on lipoprotein levels in visceral obesity. A total of 145 sedentary men, free from metabolic disorders requiring pharmacotherapy, were classified into two groups on the basis of their apo A-II-MspI genotype determined by the polymerase chain reaction: 1) 43 M1 carriers or M1M2, including two M1M1 homozygotes and 41 M1M2 heterozygotes, and 2) 102 M2M2 homozygotes for the presence of a MspI restriction site. The two genotypic groups did not differ for body mass index (BMI, expressed in kg/m2), body fat mass, visceral adipose tissue (AT) accumulation, as well as for insulin, glucose and free fatty acids levels measured in the fasting state and in response to an oral glucose tolerance test. In addition, 65 and 63% of M1 carriers had plasma HDL2 cholesterol levels and a HDL2/HDL3 cholesterol ratio below the 50th percentile of their distributions compared with 45%(P < 0.05) and 46%(P = 0.06), respectively, in M2M2 homozygotes. When subjects were further divided on the basis of visceral AT accumulation (below and above a value of 130 cm2), M1 carriers with low levels of visceral AT were characterized by high plasma HDL cholesterol and HDL2 cholesterol concentrations as well as by a higher HDL2/HDL3 ratio, compared with M1 carriers with high levels of visceral AT (> 130 cm2), or with M2M2 homozygotes with either a high or a low accumulation of visceral AT. Furthermore, M1 carriers with high levels of visceral AT showed a trend for lower plasma HDL2 cholesterol levels and were characterized by a significantly lower HDL2/HDL3 cholesterol ratio compared with the other three groups. No difference in HDL and HDL2 cholesterol levels and in the HDL2/HDL3 cholesterol ratio was noted when M2 homozygotes with lower versus higher levels of visceral AT were compared. The contribution of hyperinsulinemia was also examined by dividing subjects on the basis of the 50th percentile of the integrated insulin response to an oral glucose challenge. Significantly lower plasma HDL2 cholesterol levels and a reduced HDL2/HDL3 cholesterol ratio were noted among M1 carriers with high plasma insulin responses compared with M1 carriers with low insulin responses. Among M2M2 homozygotes, no difference was noted in plasma HDL cholesterol and in HDL2 cholesterol concentrations between men with low versus high insulin responses to the oral glucose load. These results suggest that the apo A-II-MspI polymorphism could modulate plasma HDL cholesterol levels among visceral obese, insulin-resistant men.
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PMID:The MspI polymorphism of the apolipoprotein A-II gene as a modulator of the dyslipidemic state found in visceral obesity. 905 Jul 75

Plasma lipoprotein cholesterol abnormalities, diabetes, hypertension and smoking have all been identified as independent predictors of cardiovascular events. Clustering of multiple risk factors suggests a common metabolic link among high blood pressure, insulin resistance, plasma lipoprotein abnormalities and obesity. New guidelines for the management of dyslipidemias target patients with established coronary artery disease (CAD), and high risk patients with multiple risk factors and severe genetic lipoprotein disorders, such as familial hypercholesterolemia. To determine the prevalence of lipoprotein, apolipoprotein and metabolic disorders in premature CAD, 243 men and 61 women with premature CAD (occurring before age 60 years) and 203 age- and sex-matched controls (152 men, 61 women) were studied. After correcting for beta-blocker use (40% of men and 54% of women), hypertension and diabetes were seen more frequently in CAD patients than in controls. In men and women, cholesterol, triglycerides, low density lipoprotein (LDL) cholesterol, apolipoprotein B and lipoprotein (a) were significantly higher, and high density lipoprotein (HDL) cholesterol was lower, in CAD patients than in controls. By stratifying patients according to LDL cholesterol: HDL cholesterol ratio (5 or less, or greater than 5) and by triglyceride levels (less than 2.3 mmol/L, or 2.3 mmol/L or greater), significantly more men and women with CAD were found to have an elevated LDL cholesterol:HDL cholesterol ratio and elevated triglycerides (13.8% versus 1.9%, men and women combined, CAD versus controls, P < 0.0001). A metabolic factor index was devised, assigning a score of 1 each for presence of hypertension, lipoprotein abnormalities, diabetes or fasting blood glucose above 7.0 mmol/L, and a body mass index of 27 or greater. The prevalence of a metabolic factor index of 3 or more was 29.2% in CAD men versus 6.7% in controls (P < 0.0001) and 38.3% in CAD women versus 11.7% in controls (P < 0.01). Familial hypercholesterolemia was seen in fewer than 5% of patients with premature CAD and type III dyslipoproteinemia in one of 343 CAD patients. The distribution of apolipoprotein E phenotypes was the same in CAD patients and controls. Multivariate analysis revealed that in men, HDL cholesterol, lipoprotein (a) levels and smoking were the best predictors of risk. In men, plasma levels of LDL cholesterol, triglycerides or body mass index did not enter the model at the P < 0.05 level. In women, low HDL cholesterol, lipoprotein (a), the presence of diabetes, smoking and apolipoprotein B levels were all predictors of risk (P < 0.05). However, the clustering of risk factors may be the best predictor of risk. In this selected population, HDL and lipoprotein (a) are the best metabolic markers of premature CAD; metabolic factor clustering is common in patients with premature CAD.
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PMID:Metabolic factors clustering, lipoprotein cholesterol, apolipoprotein B, lipoprotein (a) and apolipoprotein E phenotypes in premature coronary artery disease in French Canadians. 911 13

To understand the effects of the interaction between genetic polymorphisms and obesity on the risk of hypertriglyceridemia (HTG), two polymorphisms, an SstI polymorphism on the apolipoprotein CIII gene and a HindIII polymorphism on the lipoprotein lipase gene, were analyzed in 339 Chinese subjects with (82 cases in the HTG group) or without HTG (257 cases in the control group). Our data revealed that the frequencies of obesity, the SstI minor allele (S2), and the HindIII major allele (H+) in the HTG group were significantly higher than in the control group. Subgroup analysis revealed that the association between these two polymorphisms and HTG occurred predominantly in nonobese subjects and in subjects with the less hypertriglyceridemic genotype of another polymorphism. Multivariate logistic regression analysis showed that all three risk factors (obesity, S2-containing chromosome, and H+ homozygosity) were associated with HTG, and an interaction was found between obesity and H+ homozygosity for the occurrence of HTG. The risk of HTG increased significantly with combinations of risk factors. Subjects can be divided into low or high risk groups for HTG using such combinations. These results provide evidence of interaction between obesity and the HindIII polymorphism of the lipoprotein lipase gene on the risk of HTG.
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PMID:Interaction between obesity and genetic polymorphisms in the apolipoprotein CIII gene and lipoprotein lipase gene on the risk of hypertriglyceridemia in Chinese. 927 50

This paper reviews evidence supporting the notion that genetic factors may have an influence on the determination of body fat distribution, particularly emphasizing the genetic susceptibility of visceral adipose tissue (AT) accumulation. The potential contribution of genetic susceptibility to the development of metabolic alterations in visceral obese individuals will also be reviewed. The contribution of genetic factors to the variation in body fat distribution is supported by studies in which racial differences in body fat distribution were reported. These ethnic differences suggest that body fat distribution may be influenced by some components of the genetic background which are shared among individuals of a given race. Furthermore, the familial aggregation and the resemblance between monozygotic twins that have been observed for anthropometric measurements of body fat distribution and for visceral AT accumulation measured by computed tomography, also suggest that genetic factors are involved in the determination of body fat distribution. Genetic susceptibility may also influence the relationship between visceral AT accumulation and the development of metabolic alterations. In this regard, it has been reported that the polymorphism of some genes (for example, the apolipoprotein (apo) E, apo B100 and lipoprotein lipase genes) is altering the relationship between visceral obesity and plasma lipoprotein-lipid levels. In conclusion, results presented in this paper suggest that genetic factors seem to have a significant influence on the propensity to accumulate AT in the visceral depot and that genetic factors also seem to affect the associations commonly reported between visceral obesity and the development of metabolic alterations.
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PMID:Genetic susceptibility to visceral obesity and related clinical implications. 934

Apolipoprotein is now a new biochemical marker for evolution of atherosclerosis, even better than lipid fraction. We studied seric apolipoprotein A and B (Apo A, B) on 50 cases with complicated obesity, with ages between 37-52 years, and 15 males and 35 females. Selection criteria were: android constitution, obesity, essential hypertension (EHT). We also made statistical correlations on IBM PC compatible computer using chi-square test. We correlated glycoregulation abnormalities with body mass index (BMI > 25) with meaningfully value (p < 0.005) or with complicated EHT less meaningfully (p < 0.2). On this background, we appreciated the predictive value of seric levels of Apo A, B and Apo B/A ratio > 1. EHT correlates with low levels of seric Apo A very meaningfully (p < 0.0001) and this association is higher correlated when added ICD (P < 0.00001). There is no significant relationship between high levels of seric Apo B and EHT in our study, but it is significant for Apo B/A > 1 (p < 0.0001). EHT with seric cholesterol are not correlated (p:NS). Our conclusion is that seric Apo A and Apo B/A are statistical predictive risk factors for complicated EHT on android obese persons (X syndrome).
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PMID:[Apolipoproteins-a cardiovascular risk factor within the context of syndrome X]. 945 12

To examine the association of hyperinsulinemia with the atherogenic risk profile in children, we studied the relationships of the fasting plasma insulin level with indices of obesity (body mass index [BMI] and sum of triceps and subscapular skinfold thickness [SFT]), body fat distribution (waist to hip ratio [WHR]), serum lipid, lipoprotein, and apolipoprotein levels, and blood pressure in a case-control study of 460 Kuwaiti prepubertal obese children aged 6 to 13 years matched by age and sex to 460 prepubertal non-obese controls. Obese children were ascertained in a representative cross-sectional study of 2,400 school children. Fasting insulin levels were positively correlated (P < .001) with serum triglyceride (TG) and very-low-density lipoprotein (VLDL) cholesterol levels and negatively correlated with high-density lipoprotein (HDL) cholesterol levels. No significant associations were observed between insulin and total cholesterol (TC), cholesterol, low-density lipoprotein (LDL) or apolipoprotein A-I (apo A-I). Stronger associations of insulin levels with lipoprotein fractions were observed in obese versus non-obese controls. Obese children had a higher concentration of apo B and a lower apo A-I:B ratio (P < .001). Insulin and the insulin to glucose ratio increased with age in obese children, whereas there were slight changes in non-obese children. TG and HDL cholesterol levels and systolic blood pressure (SBP) were significantly different across insulin quartiles in boys and girls. We conclude that the fasting plasma insulin level may be used as a marker for the development of obesity-associated metabolic disorders and elevated blood pressure in children.
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PMID:Association of fasting insulin with serum lipids and blood pressure in Kuwaiti children. 955 May 39

The influence of obesity and fat distribution on serum levels of lipoprotein and apolipoprotein was investigated in 294 Japanese junior high school children (12-13 years of age). Serum levels of low-density lipoprotein cholesterol (LDLC) (P = 0.013), triglycerides (TG) (P = 0.0006), and apolipoprotein B (apoB) (P = 0.003), and the apoB/A-I ratio (P = 0.005) were significantly higher and serum levels of high-density lipoprotein cholesterol (HDLC) (P = 0.00003) and apoA-1(P = 0.003) were significantly lower in obese boys than in non-obese boys. The serum levels of TG (P = 0.013) and the apoB/A-I ratio (P = 0.011) were significantly higher and the serum levels of HDLC (P = 0.004) was significantly lower in obese girls than in non-obese girls. The LDLC/apoB ratio was lower in obese girls than in non-obese girls (P = 0.03). Obesity (> or = 20% of ideal weight) was strongly correlated with the serum levels of lipids and apolipoproteins in boys; this relationship was less clear in girls. The degree of obesity and the body mass index (BMI) were more strongly correlated with serum levels of lipids and apolipoproteins in boys than in girls. In boys, atherogenic lipoproteins and apolipoproteins, such as LDLC and apoB, showed a stronger correlation with the thickness of the triceps skinfold, while in girls the anti-atherogenic lipoproteins and apolipoproteins, such as HDLC and apoA-I, showed a stronger correlation with both the triceps and the subscapular skinfold thicknesses. In girls the relationships between the BMI and the degree of obesity and the thickness of the subscapular skinfold (S) thickness were similar to the relationships between those parameters and the triceps skinfold (T) thickness. In boys, these parameters showed a stronger correlation with the subscapular skinfold thickness than with the triceps skinfold thickness. The correlation coefficients for the relationships between skinfold thickness and lipid and apolipoprotein levels were similar to the coefficients for the relationships between skinfold thicknesses and the severity of obesity and the BMI. The distribution of central-type fat accumulation, which is indicated by the thickness of the subscapular skinfold, the S/T ratio and S-T value, was inversely correlated with the HDLC level in both boys and girls. The degree of obesity was strongly correlated with the atherogenic lipoprotein profile in boys, in part because the subscapular skinfold thickness was strongly correlated with the degree of obesity and the BMI. In girls, the correlations between indices of central-type obesity and atherogenic lipid and apolipoprotein profiles were stronger than in boys. These data suggest that childhood obesity may be an early cardiovascular risk factor.
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PMID:Relationship between fat distribution and lipid and apolipoprotein profiles in young teenagers. 958 98

To evaluate the interrelationships among body composition, blood pressure, and lipid phenotypes in adolescent black and white boys, we assessed racial distributions of lipids, blood pressure, and obesity and their joint occurrence in black and white boys aged 10 to 15 years. Subjects were recruited from Cincinnati (OH) schools. Because the differences in high-density lipoprotein cholesterol (HDL-C) and triglycerides (TGs) are the most profound coronary heart disease (CHD) risk factor differences between black and white males, we assigned subjects to one of four low-HDL-C and high-TG categories (normal and increased risk) using the age/race-specific 25th (HDL-C) and 75th (TG) percentiles. We then assessed racial distributions of lipids, blood pressure, and obesity by these phenotypes. Age differences between the black and white participants were significant, with the former about 3 months younger (P=.03), but black boys were more mature and were significantly taller and heavier and had a greater body mass index ([BMI] weight in kilograms divided by height in centimeters squared). Differences in the sum of the triceps, subscapular, and suprailiac skinfolds were not significant. Blacks had significantly higher HDL-C, lower TG, and higher diastolic blood pressure (DBP), but differences in systolic blood pressure (SBP) were not significant. In both racial groups, the body composition measures were significantly correlated with HDL-C, TG, and blood pressure levels; the correlations between HDL-C and both weight and BMI were significantly stronger in white boys. The proportion of boys of each race with low HDL-C and high TG was similar by design. In both racial groups, subjects with the conjoint trait had a significantly greater BMI, triceps skinfold, and sum of skinfolds than subjects in the other phenotypic groups. For white boys, participants with the conjoint trait had the highest SBP and DBP; differences in SBP were significant for comparisons to the normal- and high-TG group alone, and differences in DBP were significant for the comparison between normal and low HDL-C alone. For black boys, subjects with both normal HDL-C and TG had significantly lower SBP than boys with either the conjoint trait or high TG alone; none of the group differences in DBP were significant. Black had significantly less dense LDL (more LDL-C per apolipoprotein [apo] B). In each racial group, boys with the conjoint trait had the most dense LDL, significantly more dense than in any of the other phenotypes in black boys and significantly more dense than in boys with low HDL-C alone and normal boys in the white group. In both racial groups, the occurrence of no risk factors (>75th percentile TG, BMI, SBP, and DBP or <25th percentile HDL-C) and three or more risk factors was greater than expected by chance alone, and the occurrence of exactly one risk factor and two factors was less. When examined by phenotypic groups within race, boys in each racial group with the normal phenotype had a greater than expected percentage with no risk factors, and white boys with the conjoint trait were more likely to have a marked increase in multiple risk factors. Possible mechanisms for this clustering of risk factors and for the racial differences in the patterns are discussed.
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PMID:The conjoint trait of low high-density lipoprotein cholesterol and high triglycerides in adolescent black and white males. 959 40

The adipocyte hormone leptin activates signal transducer and activator of transcription 3 (STAT3) in the hypothalamus, mediating increased satiety and increased energy expenditure. To date, leptin-mediated activation of the STAT pathway in vivo has not been established in tissues other than hypothalamus. We now describe leptin receptor expression and in vivo signaling in discrete regions of the mouse gastrointestinal tract. Expression of the functional isoform leptin receptor (OB-Rb) is restricted to the jejunum and is readily detected by RT-PCR in isolated enterocytes from this site. Intravenous injection of leptin rapidly induced nuclear STAT5 DNA binding activity in jejunum of +/+ and obese (ob/ob) mice but had no effect in the diabetic (db/db) mouse that lacks the OB-Rb isoform. In addition, an induction of the immediate-early gene c-fos is observed in jejunum in vivo. Leptin-mediated induction of a number of immediate-early genes and activation of STAT3 and STAT5 in a human model of small intestine epithelium, CACO-2 cells, corroborate this effect. Furthermore, intravenous leptin administration caused a significant 2-fold reduction in the apolipoprotein AIV transcript levels in jejunum 90 min after a fat load. Our results suggest that the epithelium of jejunum is a direct target of leptin action, and this activity is dependent on the presence of OB-Rb. Lack of leptin or resistance to leptin action in this site may contribute to obesity and its related syndromes by directly affecting lipid handling.
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PMID:Leptin action in intestinal cells. 974 2

Abnormalities of plasma high density lipoprotein (HDL) levels commonly reflect altered metabolism of the major HDL apolipoproteins, apoA-I and apoA-II, but the regulation of apolipoprotein metabolism is poorly understood. Two mouse models of obesity, ob/ob and db/db, have markedly increased plasma HDL cholesterol levels. The purpose of this study was to evaluate mechanisms responsible for increased HDL in ob/ob mice and to assess potential reversibility by leptin administration. ob/ob mice were found to have increased HDL cholesterol (2-fold), apoA-I (1.3-fold), and apoA-II (4-fold). ApoA-I mRNA was markedly decreased (to 25% of wild-type) and apoA-II mRNA was unchanged, suggesting a defect in HDL catabolism. HDL apoprotein turnover studies using nondegradable radiolabels confirmed a decrease in catabolism of apoA-I and apoA-II and a 4-fold decrease in hepatic uptake in ob/ob mice compared with wild-type, but similar renal uptake. Low dose leptin treatment markedly lowered HDL cholesterol and apoA-II levels in both ob/ob mice and in lean wild-type mice, and it restored apoA-I mRNA to normal levels in ob/ob mice. These changes occurred without significant alteration in body weight. Moreover, ob/ob neuropeptide Y-/- mice, despite marked attenuation of diabetes and obesity phenotypes, showed no change in HDL cholesterol levels relative to ob/ob mice. Thus, increased HDL levels in ob/ob mice reflect a marked hepatic catabolic defect for apoA-I and apoA-II. In the case of apoA-I, this is offset by decreased apoA-I mRNA, resulting in apoA-II-rich HDL particles. The studies reveal a specific HDL particle catabolic pathway that is down-regulated in ob/ob mice and suggest that HDL apolipoprotein turnover may be regulated by obesity and/or leptin signaling.
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PMID:Increased high density lipoprotein (HDL), defective hepatic catabolism of ApoA-I and ApoA-II, and decreased ApoA-I mRNA in ob/ob mice. Possible role of leptin in stimulation of HDL turnover. 993 8

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