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)

Nine obese women with oligo- or ameno-rrhoea, all with clinical and endocrinological signs of polycystic ovary syndrome (PCO) were submitted to metabolic studies. Their mean weight was 96 kg and their mean plasma testosterone concentration was 3.5 nmol/l. A group of nine obese, regularly menstruating women of similar age and degree of obesity (mean body weight 102 kg) served as controls. Their mean testosterone concentration was 1.9 nmol/l. The high-density lipoprotein (HDL) cholesterol and apolipoprotein (apo) A-I concentrations in plasma were significantly lower in women with PCO than in control women. Furthermore, in the whole group the testosterone level showed significant inverse relationships to HDL-cholesterol (r = -0.64; P less than 0.01) and apo A-I (r = -0.59; P less than 0.01). The lipoprotein lipase activity (LPLA) in adipose tissue was lower in the women with PCO than in the control group with levels similar to those found in adipose tissue in men. There was an inverse relationship between the testosterone concentration in plasma and LPLA in adipose tissue (r = -0.51; P less than 0.05). The fat cells were of similar size at different regions in the women with PCO but showed marked differences in the control subjects who had much larger cells at the femoral than the abdominal site. The results show that the hyperandrogenism in PCO affects adipose tissue LPLA which could explain the lower HDL cholesterol values in women with PCO.
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PMID:Metabolic profile in obese women with the polycystic ovary syndrome. 310 51

The purpose of this study was to elucidate the relationship between two genetic factors associated with raised blood cholesterol, i.e. familial hypercholesterolemia (FH) and apolipoprotein (apo) E4. A group of 50 unrelated heterozygous FH patients aged 33-71 years were studied together with 129 normolipidemic subjects. A significantly higher frequency of apo E4 phenotypes was found in FH patients (30.0%) than in normolipidemic subjects (15.5%). FH patients were divided into two groups with and without apo E4. Plasma total cholesterol (Chol) and triglyceride (TG) levels were significantly higher, and plasma low density lipoprotein-cholesterol (LDL-Chol) level tended to be higher in FH patients with apo E4 than in those without apo E4. In addition, the prevalence of ischemic heart disease (IHD) was significantly higher in FH patients with apo E4 (73.3%) than in those without apo E4 (31.4%). No significant difference was noted in age and in the prevalence of obesity, diabetes, hypertension and smoking between the FH groups with and without apo E4. These results suggest that apo E4 is associated with higher levels of total Chol and TG and, at least in part, contributes to the predisposition to IHD in FH.
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PMID:Familial hypercholesterolemia and apolipoprotein E4. 321 64

Recent studies have related waist to hip ratio (WHR) to the incidence of coronary heart disease (CHD), but the causes underlying this relation are not fully known. The purpose of this study was to determine if waist to hip ratio is associated with the concentration of plasma lipids and apolipoproteins (apoproteins) that predispose individuals to a higher CHD risk. Plasma lipids and apoprotein concentrations were determined in 100 male volunteers, ranging in age from 19-68 yr, and WHR ranging from 0.89-1.09. Significant positive associations were found between WHR, plasma glucose (r = 0.25, P = 0.01), cholesterol (r = 0.21, P = 0.04), LDL cholesterol (r = 0.22, P = 0.03), triglycerides (r = 0.25, P = 0.01) and the ratio of total cholesterol to HDL-cholesterol (r = 0.30, P = 0.002). Negative associations were found between WHR and HDL-cholesterol (r = -0.19, P = 0.05), plasma apoprotein A-I (4 = -0.28, P = 0.005) and the ratio of plasma apoprotein A-I to apoprotein B (r = -0.26, P = 0.01). To determine the extent to which these correlations were independent of age and body fat content, a subsample of 15 pairs matched on age and percent body fat, but differing in WHR was selected from the larger sample. In the group with high WHR (1.06) HDL-cholesterol and apo A-I levels were lower and apo B higher than in the group with low WHR (0.96). Total cholesterol, triglycerides and LDL cholesterol levels in the group with high WHR were also higher but marginally significant statistically. These results show that WHR is associated with plasma lipid and apolipoprotein concentrations that are more predisposing to CHD and that males with male type obesity may be at a higher risk of CHD development than those with female type, regardless of age or degree of obesity.
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PMID:Body fat distribution, plasma lipoproteins and the risk of coronary heart disease of male subjects. 323 66

A summary of the lipoprotein and carbohydrate risk factors for coronary heart disease associated with use of oral contraceptives is followed by a discussion of the methodological difficulties in measuring them, and then by a description of the properties of commonly used oral steroids. Impaired glucose tolerance, high insulin levels, reduced HDL cholesterol and increased LDL cholesterol and VLDL triglycerides are features of coronary heart disease, diabetes, obesity and use of oral contraceptives. A more accurate assessment of glucose tolerance may be measurement of the plasma C-peptide of insulin. Lipid risk factors are subject to wide individual variation as well as special difficulties for pill users. For example, the convenient dextran sulfate method of precipitating HDL, from which the LDL value is calculated, may not be accurate for pill takers because of elevated triglycerides. Even assay of apolipoprotein B is subject to this distortion. If apolipoprotein methods can be standardized, assay of apolipoprotein A1, corresponding to the HDL2 subclass, may be appropriate. Progestins of the gonane class, such as levonorgestrel, because of their androgenic activity, induce changes in lipid risk factors in women similar to those of men. The net effect of the combination of estrogen and progestin is what matters, however. Although progestin-only pills have no effect on carbohydrate metabolism, combined pills decrease glucose tolerance with time, induce hypertriglyceridemia, and oppose the tendency of the estrogen to increase HDL. Norethindrone or other estrane compounds have less impact. Data on triphasics are sparse, but suggest a lesser effect also. New progestins with lower androgenic effects are being developed, although they may confer the added risk of increased triglycerides. Parenteral steroid administration or use of natural hormones are potential solutions.
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PMID:Oral contraceptives and coronary heart disease: modulation of glucose tolerance and plasma lipid risk factors by progestins. 328 33

Type V hyperlipoproteinemia is characterized by elevations of chylomicron (CM) and very low density lipoprotein (VLDL) triglycerides. The development of this lipid disorder involves a multitude of metabolic derangements including deficient clearance of triglycerides and/or their increased output aggravated by obesity, diabetes, alcohol intake, or use of some hormones. Some studies have suggested that the apolipoprotein E4 phenotype is involved in this dyslipoproteinemia but this concept is still a matter of controversy. Therefore, we determined the apoE phenotype in 21 patients with severe hypertriglyceridemia classified as type V. Their apoE4 gene frequency was 0.595 which is 2.6-fold higher (P less than 0.001) than that in the Finnish population. Correspondingly, their apoE3 gene frequency was lower than that in the normal population. No differences were noted in plasma lipoproteins of the apoE4 phenotypes and the other type V subjects. The apolipoprotein C-II and C-III distribution was similar to that in normolipidemic subjects. The results suggest that apoE4 may be involved in the development of type V hyperlipoproteinemia.
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PMID:Role of apolipoproteins E and C in type V hyperlipoproteinemia. 337 42

The lipid transport system of 3-month-old male C57BL/6J obese (ob/ob) mice was investigated. Serum lipoproteins were separated by density gradient ultracentrifugation and characterized by their chemical and electrophoretic properties as well as their relative apolipoprotein contents, defined according to molecular weight and charge. Obese, ob/ob mice exhibited a marked hyperlipoproteinemia resulting from large increases in low-density lipoproteins (LDL, d 1.021-1.058 g/ml) and high-density lipoproteins (HDL, d 1.058-1.137 g/ml), particularly, the HDL2 subclass (d 1.058-1.109 g/ml). This increase in lipoproteins was entirely responsible for their hypercholesterolemia and hyperphospholipidemia. By contrast, these obese mice had a net decrease in very-low-density lipoproteins (VLDL, d less than 1.016 g/ml) and intermediate-density lipoproteins (IDL, d 1.016-1.021 g/ml), which accounted for their moderate hypotriglyceridemia. The chemical composition of heterogeneous light LDL (d 1.021-1.040 g/ml and dense LDL (d 1.040-1.058 g/ml) overlapped by HDL-like particles was highly modified. These modifications consisted of increases in the percentages of cholesteryl ester and phospholipid and decreases in that of triacylglycerol. There were also marked changes in the relative values of the apolipoproteins of VLDL, but principally, IDL and LDL. IDL and light LDL were poorer in apolipoproteins BH (Mr 340,000-320,000) and eventually in apolipoprotein BL (Mr 220,000-200,000) and enriched in apolipoproteins E (Mr 37,000-35,000) and C-A-II (Mr approximately equal to 12,000). A similar and very significant change occurred in VLDL for both the apolipoproteins BL and C-A-II. Dense LDL, mainly poorer in apolipoprotein BH and enriched in apolipoprotein A-I (Mr 28,000-27,000), closely resembled HDL2 in all the groups, and were enriched in apolipoproteins C-A-II in only the obese mice. We suggest that ob/ob mice are probably protected against atheromata because of the low VLDL and IDL levels, and the increase in HDL2.
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PMID:Serum lipoprotein and apolipoprotein profiles of the genetically obese ob/ob mouse. 338 93

During the period January 1979-March 1983, we have conducted in Jerusalem a case control study of all patients under the age of 65 surviving their first diagnosed myocardial infarction, in order to evaluate the importance of the conventional risk factors and to detect additional factors through quantifying plasma apolipoprotein concentrations. As a control group, we have chosen a sample from a previously studied Jewish population (LRC study), representative of the adult Jerusalemite population, parents of children born during 1958-1961. To complete the younger age group missing in the LRC population, we added a population studied in the Kiryat Yovel district of Jerusalem. We report here the results obtained from interviews and analysis of 532 cases (448 males and 84 females), and 869 controls (457 males and 412 females). In order to overcome the effects of age and ethnic origin on the risk factors, we have divided our populations according to age and country of origin of their fathers. Age, sex, smoking, history of high blood pressure, diabetes, elevated plasma triglycerides and/or cholesterol, and decrease in plasma HDL cholesterol, emerged as the most powerful and significant risk factors in this study. Other putative risk factors such as socioeconomic status, dietary habits, physical activity and obesity index were not found to be significantly different between cases and controls. It is noteworthy that smoking was more important as a risk factor in the younger age groups, whereas hypertension and diabetes were more important in the older age groups, particularly in females. The differences in lipid levels were considerably more prominent in the young age groups in both sexes. Myocardial infarction was observed more frequently in patients of European or American extractions. Apolipoproteins A-I, A-II, E and B determined in this study were shown to be affected partly by age and country of origin. Apo E and apo B levels were significantly higher and Apo A-I significantly lower in patients with myocardial infarction when compared to controls.
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PMID:Analysis of risk factors in 532 survivors of first myocardial infarction hospitalized in Jerusalem. 345 28

To understand the relationship between very low-density lipoprotein (VLDL) triglyceride and VLDL apolipoprotein (apo) B, we studied their metabolisms simultaneously in 53 subjects with a range of obesity and glycemia. Obese subjects had increased production of both VLDL apo B and VLDL triglyceride and more VLDL of normal composition. Compared with nondiabetics, diabetic subjects had decreased clearance of both VLDL apo B and VLDL triglyceride, increased production of VLDL triglyceride but not of VLDL apo B, and more VLDL of abnormal composition. Production of both VLDL apo B and VLDL triglyceride were significantly correlated with plasma insulin concentrations, and rates of clearance of both were inversely correlated with plasma glucose. There was no direct correlation between total plasma free fatty acid concentration and production of either VLDL triglyceride or VLDL apo B, but VLDL triglyceride production was found to account for only a very small proportion of the nonoxidative component of free fatty acid turnover. We suggest that in obese subjects hyperinsulinemia induces overproduction of both VLDL apo B and VLDL triglyceride. In diabetes VLDL is increased in part because of decreased clearance; the altered composition is the result of the increase in VLDL-triglyceride production independent of apo B. The increase in VLDL triglyceride production may be mediated through plasma free fatty acids or glucose, although assessment of the relationship between these precursors and VLDL triglyceride is confounded by the fact that only a small portion of free fatty acids or glucose is converted to VLDL triglyceride.
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PMID:Coordination of very low-density lipoprotein triglyceride and apolipoprotein B metabolism in humans: effects of obesity and non-insulin-dependent diabetes mellitus. 354 65

Serum lipid, lipoprotein cholesterol, and apolipoprotein (A-I and B) levels were compared between 940 black and 1710 white children who were between the ages of 5 and 17 years. Stratification, matching, and analysis of covariance were used to determine whether black-white differences in levels of serum triglycerides (TG), very low- (VLDL-C), and high- (HDL-C) density lipoprotein cholesterol, and apolipoprotein A-I (apoA-I) could be explained by differences in sexual maturation, obesity, cigarette smoking, alcohol intake, oral contraceptive use, insulin, and glucose. Independently of these covariates, blacks had elevated levels of HDL-C and apoA-I (males only), and whites had increased levels of TG and VLDL-C. All differences were statistically significant at the 0.001 level. In addition, racial contrasts tended to be greater in sexually mature, as compared with prepubertal, males; a similar divergence of levels with sexual maturation was not observed in females. HDL-C levels in white males were partially explained (R2 = 0.12) by sexual maturation, insulin, and obesity; apoA-I levels were associated with only sexual maturation and insulin. Racial differences in levels of serum lipids, lipoprotein cholesterol, and apoA-I in early life, therefore, exist independently of differences in several lipoprotein determinants. Since the initial stages of atherosclerosis begin in the young, these black-white lipoprotein contrasts may influence differences in adult coronary heart disease rates between the races.
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PMID:Black-white differences in serum lipoproteins during sexual maturation: the Bogalusa Heart Study. 355 7

The relationship of serum lipoprotein and apolipoprotein concentrations to angiographically determined coronary artery disease was investigated in 105 consecutive male survivors of myocardial infarction under the age of 45. Concentrations and composition of lipoproteins, lipid indexes, and nonlipid risk factors (tobacco consumption, hypertension, reduced glucose tolerance, and obesity) were related to a recently developed scoring system for semiquantitative estimation of diffuse coronary atheromatosis, as well as to the number and severity of significant coronary artery stenoses. The concentrations of cholesterol in very low-density lipoprotein (VLDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL), in combination with serum triglyceride or VLDL triglyceride level, comprised the best set of independent discriminatory lipid variables between patients and control subjects. In the patients, LDL cholesterol and apolipoprotein B levels showed strong relationships to the extent and severity of coronary atheromatosis but not to the number and severity of distinct coronary stenoses. HDL2 cholesterol concentration correlated inversely with the coronary atheromatosis score, whereas other variables reflecting HDL concentration and composition or VLDL lipids were not independently related to any of the coronary scores. The LDL triglyceride level, an index of intermediate-density lipoprotein (IDL) accumulation, was significantly correlated to the coronary atheromatosis score in univariate analysis. Nonlipid risk factors were correlated neither to coronary atheromatosis nor to severity of stenoses. Stepwise multiple regression analyses of data adjusted for age, cumulative tobacco consumption, and weight indicated that 18% of the variation in the coronary atheromatosis score could be accounted for by levels of apolipoprotein B. Addition of other lipoprotein variables or the nonlipid variables hypertension and glucose tolerance did not significantly increase the value of R2. When ratios of lipoprotein lipids and apolipoproteins were included in the regression model, the highest multiple correlation coefficient was obtained with the LDL/HDL cholesterol ratio alone (R2 = .22). The present data demonstrate the importance of elevated LDL cholesterol and apolipoprotein B concentrations for the development of coronary atheromatosis in young male survivors of myocardial infarction. The lack of correlations between the levels of lipoprotein lipids and serum apolipoproteins and the severity of coronary stenoses suggests that mechanisms other than disturbances of lipoprotein metabolism may be involved in the progression of more advanced coronary lesions.
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PMID:Relationship of angiographically defined coronary artery disease to serum lipoproteins and apolipoproteins in young survivors of myocardial infarction. 369 44


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