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

Obesity is frequently associated with several alterations of plasma lipid levels and lipoprotein metabolism. To evaluate the effects of severe obesity and weight loss on plasma lipoprotein sub-class levels and composition 11 grossly obese patients were examined before and six and 12 months after gastroplasty. Plasma lipoproteins were isolated by ultracentrifugation in a zonal rotor under rate flotation conditions. Mean body weight was 121.9 kg before gastroplasty, 97.6 kg after six months, and 90.7 kg after 12 months. Total plasma cholesterol was not affected by the weight reduction. Obese patients were characterized by increased levels of IDL and small dense LDL (LDL3). LDL levels, but not LDL3, were reduced following weight reduction. Plasma apo B levels of obese patients were always higher than in controls and were not affected by the weight reduction. After 12 month's weight loss total HDL cholesterol increased without modification of HDL sub-class cholesterol distribution, which was similar to that of normal controls. Plasma apo AI in obese patients was not affected by changes in body weight, and remained below normal. The percentage protein-lipid composition of LDL2 and HDL3 in obese patients was characterized by a decreased cholesterol ester content before gastroplasty which was normalized 12 months after gastroplasty. The presence of IDL and LDL3 in increased concentrations in severely obese patients may represent a vascular risk factor since similar abnormalities were recently observed in non-obese patients affected with vascular diseases.
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PMID:Lipoprotein sub-fraction levels and composition in obese subjects before and after gastroplasty. 132 87

High density lipoprotein subfraction 2 (HDL1)-cholesterol level is usually decreased in Type 2 (non-insulin-dependent) diabetes. A study was carried out in 251 Type 2 diabetic patients (106 males [M], 145 females [F]) and in 120 non diabetic controls in order to determine the influence of hypertriglyceridaemia and obesity on the HDL2-cholesterol level and to analyse the relationship between HDL2-cholesterol level and atherosclerosis (coronary heart disease, peripheral atherosclerosis or cerebral vascular disease), in Type 2 diabetes. Influence of hypertriglyceridaemia and obesity on HDL2-cholesterol level was studied by comparing the mean values of HDL2-cholesterol between diabetics and controls, after controlling for hypertriglyceridaemia and obesity, and by a multiple linear regression test. A stepwise logistic regression was performed to analyse the association between the prevalence of atherosclerosis and several variables: age, duration of diabetes, hypertension, cigarette smoking, body mass index, mean glycaemia, total cholesterol, triglyceride, HDL-cholesterol, HDL2-cholesterol and HDL3-cholesterol levels. In both men and women, when both of the factors (hypertriglyceridaemia and obesity) were present of when only one was, HDL2-cholesterol level was significantly lower in the diabetic population, compared with controls. But when obesity and hypertriglyceridaemia were absent, HDL2-cholesterol level, in the diabetic population, was not significantly different from controls (M: 17.9 +/- 13.3 vs 20.5 +/- 13.8 mg/dl: NS; F: 30.1 +/- 21.5 vs 27.6 +/- 14.2 mg/dl: NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of obesity and hypertriglyceridaemia on the low HDL2-cholesterol level and on its relationship with prevalence of atherosclerosis in type 2 diabetes. 145 17

The objective of this study was to determine whether a less favorable risk factor pattern for cardiovascular disease among persons with impaired glucose tolerance could be explained by fasting insulin, obesity, and/or a central distribution of body fat. Between 1984 and 1988, cardiovascular risk factors were examined cross-sectionally in Hispanic and non-Hispanic white participants in the San Luis Valley Diabetes Study who had either impaired (n = 173) or normal (n = 1,107) glucose tolerance. Sex-specific analysis of covariance models were constructed to adjust risk factor levels for age, age and insulin, and age, insulin, body mass index, and centrality index. Both males and females with impaired glucose tolerance had higher age-adjusted mean diastolic blood pressures, heart rates, uric acid levels, and triglyceride levels and lower levels of high density lipoprotein (HDL) cholesterol and HDL3 cholesterol than normal subjects; differences were significant for all risk factors except HDL cholesterol and HDL3 cholesterol in males. Differences in diastolic blood pressure in males, and differences in heart rate and triglyceride in both sexes, remained significant after adjustment for all covariates. However, differences in uric acid in males and differences in diastolic blood pressure and HDL3 cholesterol in females were attenuated to borderline significance levels. Differences in uric acid and HDL cholesterol in females were diminished to nonsignificant levels, especially after adjustment for obesity-related measures. With few exceptions, fasting insulin did not appear to play a major role in accounting for differences in these risk factors. With adjustment, ethnic differences (Hispanic vs. non-Hispanic white) were smaller and were statistically significant less often than differences observed between impaired and normal glucose tolerant groups. The authors concluded that hyperinsulinemia, obesity, and a central body fat distribution accounted for some, but usually not all, of the less favorable cardiovascular risk factor pattern found in subjects with impaired glucose tolerance.
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PMID:The roles of insulin, obesity, and fat distribution in the elevation of cardiovascular risk factors in impaired glucose tolerance. The San Luis Valley Diabetes Study. 146 70

The predictors of premature coronary atherosclerosis were examined in 203 patients (99 men aged less than or equal to 50 years, and 104 women aged less than or equal to 60 years) undergoing elective diagnostic coronary arteriography. Age, cigarette smoking, hypertension, obesity, diabetes, positive family history of premature coronary artery disease (CAD), and plasma levels of total cholesterol, triglyceride, lipoproteins (i.e., very low, intermediate-, low-, and high-density [HDL] lipoproteins and their subfractions [HDL2 and HDL3], and lipoprotein [a]) and apolipoproteins (apoA-1, apoA-2 and apoB, respectively) were examined using univariate analyses and multivariate logistic regression. In men, age (p less than 0.05), smoking (p less than 0.05), and plasma triglyceride (p less than 0.02) and apoA-1 (p less than 0.05) levels were independently associated with CAD. In women, smoking (p less than 0.001) and plasma apoB levels (p less than 0.04) were the strongest variables independently associated with CAD. It is concluded that the "nontraditional" risk factors (plasma apoA-1 and apoB levels) are better predictors of premature CAD than are plasma lipoproteins and that smoking is the strongest of the traditional nonlipid risk factors.
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PMID:Comparison of the plasma levels of apolipoproteins B and A-1, and other risk factors in men and women with premature coronary artery disease. 156 71

Mexican-Americans represent the single largest component of the US Hispanic population and have been shown to bear a disproportionate burden of chronic disease. A representative sample of 1,004 Mexican-Americans aged 15-74 years from Starr County, Tex., was recruited for this study. Each subject was provided a detailed physical evaluation that included measurement of fasting levels of cholesterol, triglycerides, high density lipoprotein (HDL) cholesterol and its subfractions (HDL2 and HDL3) alpha- and beta-lipoprotein cholesterol, and low density lipoprotein cholesterol. Apolipoproteins A-I, A-II, B, C-II, C-III, and E were determined for approximately 550 of these individuals. Age- and sex-specific mean levels and percentile cut points are presented. The distributions of lipoproteins are quite similar to those of the general population except for consistently higher triglycerides in males and females and lower HDL cholesterol levels in females. These findings are consistent with the high frequency of obesity. Comparative age- and sex-specific data for the apolipoproteins are not widely available. Where such data exist, apolipoprotein levels observed in the Mexican-American population tend to be similar to or lower than the comparative data.
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PMID:Lipoprotein and apolipoprotein levels among Mexican-Americans in Starr County, Texas. 198 89

We studied the association of obesity with lipid and lipoprotein concentrations in 92 patients (49 men, 43 women) with insulin-dependent diabetes (IDDM), in 305 patients (152 men, 153 women) with non-insulin-dependent diabetes (NIDDM), and in 122 nondiabetic control subjects (65 men, 57 women). Obesity (body mass index, BMI) was associated with abnormal lipid and lipoprotein levels only in the presence of diabetes, and lipid and lipoprotein changes were substantially more abnormal in patients with NIDDM than in patients with IDDM. In men and women with NIDDM, obesity was associated with low high-density lipoprotein (HDL) and HDL2 cholesterol and high total, low-density lipoprotein (LDL), and very low-density lipoprotein (VLDL) triglyceride concentrations. In men with IDDM, obesity was related only to low HDL and HDL2 cholesterol and in women with IDDM to low HDL3 cholesterol. BMI and diabetes status had a statistically significant interaction (analysis of variance) with respect to HDL and HDL2 cholesterol and total and VLDL triglycerides, indicating that the effects of obesity on lipids and lipoproteins were more severe in patients with diabetes than in nondiabetic subjects. In conclusion, obesity and diabetes status have an unfavorable interaction that results in multiple pathologic lipid and lipoprotein changes, particularly in NIDDM.
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PMID:Adverse effects of obesity on lipid and lipoprotein levels in insulin-dependent and non-insulin-dependent diabetes. 229 84

Adipose tissue is a major cholesterol storage organ in man, and turnover of this slowly exchangeable pool is dependent on low and high density lipoproteins which deliver and remove cholesterol from this site. To determine whether lipoprotein binding is altered in the obese state, we examined the binding of low density lipoprotein (LDL) and high density lipoprotein (HDL2 and HDL3) to purified adipocyte plasma membranes obtained from omental fat depots of massively obese patients (BMI greater than 40 kg/m2) and lean subjects. The specific binding and uptake of 125I-HDL2 and 125I-HDL3 were greater for obese than for lean adipocytes. Scatchard analysis of binding studies using purified adipocyte plasma membranes and varying amounts of labeled HDL2 or HDL3 demonstrated a higher binding affinity (lower Kd) for HDL2 and higher binding capacity (Bmax) value for both HDL2 and HDL3 in obese as compared to lean. 125I-LDL specific binding was somewhat lower in obese than in lean membranes but this difference was not statistically significant. The cholesterol content of isolated omental adipocytes expressed on a cellular basis or as the cholesterol/triglyceride ratio (mg chol/g of lipid) were similar in the obese and lean subjects. Furthermore, 125I-LDL, 125I-HDL2 or 125I-HDL3 specific binding did not correlate with cellular cholesterol content or with cholesterol/triglyceride ratio. These findings indicate that lipoprotein binding to adipocytes is altered in obesity and is characterized by up-regulation of HDL (particularly HDL2) binding with little change in LDL binding. We conclude from this study that obesity has a profound effect on the expression of HDL binding sites in human adipocytes and that LDL and HDL binding in fat cells are regulated differently.
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PMID:Effect of massive obesity on low and high density lipoprotein binding to human adipocyte plasma membranes. 258 24

Obesity is associated with significant changes in cholesterol and lipoprotein metabolism. High density lipoprotein (HDL) cholesterol is often reduced and adipose tissue cholesterol stores are increased in obese individuals. This prompted a study on the binding of HLD fractions (HDL2 and HDL3) to adipocyte plasma membranes obtained from massively obese subjects (BMI greater than 37 kg m-2) undergoing gastroplasty. Regional variation in HDL binding to these adipocyte plasma membranes was demonstrated. Membranes derived from the abdominal subcutaneous depot exhibited similar binding affinity (Kd) but higher binding capacity (Bmax) for HDL2 and HDL3 than that from the omental depot. There was significant inter-individual variation in Bmax but the amount of HDL2 or HDL3 bound to the two depots of the same individual was positively correlated (HDL2, r = 0.66, P less than 0.05; HDL3, r = 0.88, P less than 0.01). While HDL2 binding showed a higher affinity (lower Kd) than HDL3, a significant positive correlation existed between HDL2 and HDL3 binding to the same adipocyte membranes (r = 0.89, P less than 0.01). A significant inverse correlation (P less than 0.05) was also observed between HDL2 and HDL3 binding to adipocyte membranes and plasma HDL-cholesterol concentration. These results suggest that adipose tissue is an important site of HDL metabolism and the subcutaneous fat depot may play a proportionally more significant role due to its higher HDL binding capacity. It is further suggested that increased HDL binding and metabolism by the expanded adipose tissue mass may contribute to reduced plasma HDL-cholesterol levels frequently associated with obesity.
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PMID:Regional variation in high-density lipoprotein binding to human adipocyte plasma membranes of massively obese subjects. 303 43

We investigated the prevalence of carotid atherosclerosis and its association with serum lipoprotein cholesterol fractions in 412 Eastern Finnish men ages 42, 48, 54, or 60 years who were examined between February and December 1987 in the Kuopio Ischaemic Heart Disease Risk Factor Study. Carotid atherosclerosis was assessed with high-resolution B-mode ultrasonography. Of the participants, 37% had thickening of the intimal or medial layer of the arterial wall, 10% had plaques, 2% had stenosis in the right or left common carotid artery or in the carotid bifurcation, and only 51% were free of any detectable carotid atherosclerosis. The prevalence of atherosclerosis was 14.1%, 32.0%, 67.7%, and 81.9% in the four age groups, respectively. The mean age-adjusted serum low density lipoprotein (LDL) cholesterol concentration was 3.67 mmol/l (142 mg/dl) in men free of carotid atherosclerosis and 4.02 mmol/l (155 mg/dl) in those with at least intimal thickening (p = 0.003 for difference). The mean age-adjusted serum cholesterol concentration in the high density lipoprotein (HDL) fraction was 1.34 mmol/l (52 mg/dl) in the atherosclerosis-free and 1.27 mmol/l (49 mg/dl) in the atherosclerotic men (p = 0.029 for difference). There was a similar difference in both the serum HDL2 and the HDL3 cholesterol levels. Serum LDL and HDL (inverse) cholesterol were significant determinants of severity of carotid atherosclerosis in a multivariate regression model adjusting for age, obesity, plasma fibrinogen, cigarette-years, and duration of hypertension. Our data reveal the high prevalence of atherosclerosis in middle-aged Eastern Finnish men and provide further evidence of the roles of LDL and HDL cholesterol in atherosclerosis.
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PMID:Prevalence of carotid atherosclerosis and serum cholesterol levels in eastern Finland. 319 22

Human obesity is frequently associated with elevated plasma triglyceride and cholesterol concentrations and reduced high density lipoprotein (HDL) cholesterol, abnormalities that commonly revert to normal levels with weight loss. This study was undertaken to examine possible mechanism(s) associated with the changes in plasma HDL cholesterol concentrations in massively obese patients after weight loss. Ten massively obese patients (two men and eight women, age = 37.8 +/- 2.4 years) were studied before, during, and after 1 year of weight loss and weight maintenance following gastric stapling. Total cholesterol and low density lipoprotein cholesterol were within the normal range for sex and age before weight loss and did not change significantly during or after weight reduction. In the females, HDL cholesterol concentrations increased from 0.96 +/- 0.06 mmol/L to 1.23 +/- 0.3 mmol/L (mean +/- SEM, n = 8, P less than .05) with weight reduction. In the two men, plasma HDL cholesterol concentrations were, respectively, 1.22 and 0.65 mmol/L before and 1.23 and 0.98 mmol/L after weight loss. Specific binding of 125I-HDL2 and 125I-HDL3 to purified plasma membranes was determined using abdominal and omental fat depot before and after weight loss in six of the ten obese patients. An average reduction of 30% to 40% in 125I-HDL2 and 125I-HDL3 binding capacity to these membranes occurred after weight loss. Furthermore, a positive correlation (r = .65, n = 10, P less than .05) was observed between plasma HDL cholesterol and triglyceride concentrations before weight loss but not after weight loss (r = .01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Weight loss in massive obesity: reciprocal changes in plasma HDL cholesterol and HDL binding to human adipocyte plasma membranes. 337 24


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